Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells
Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an import...
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| Autor*in: |
Santibáñez-Andrade, Miguel [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022transfer abstract |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: MPI vs Fortran coarrays beyond 100k cores: 3D cellular automata - Shterenlikht, Anton ELSEVIER, 2019, chemistry, biology and toxicology as related to environmental problems, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:295 ; year:2022 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.chemosphere.2022.133900 |
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ELV057029105 |
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| 245 | 1 | 0 | |a Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells |
| 264 | 1 | |c 2022transfer abstract | |
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| 520 | |a Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. | ||
| 520 | |a Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. | ||
| 650 | 7 | |a SETD2 |2 Elsevier | |
| 650 | 7 | |a PM10 |2 Elsevier | |
| 650 | 7 | |a A549 |2 Elsevier | |
| 650 | 7 | |a Aneuploidy |2 Elsevier | |
| 650 | 7 | |a Chromosomal instability |2 Elsevier | |
| 650 | 7 | |a Mitotic spindle |2 Elsevier | |
| 700 | 1 | |a Sánchez-Pérez, Yesennia |4 oth | |
| 700 | 1 | |a Chirino, Yolanda I. |4 oth | |
| 700 | 1 | |a Morales-Bárcenas, Rocío |4 oth | |
| 700 | 1 | |a Quintana-Belmares, Raúl |4 oth | |
| 700 | 1 | |a García-Cuellar, Claudia M. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Shterenlikht, Anton ELSEVIER |t MPI vs Fortran coarrays beyond 100k cores: 3D cellular automata |d 2019 |d chemistry, biology and toxicology as related to environmental problems |g Amsterdam [u.a.] |w (DE-627)ELV002112701 |
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10.1016/j.chemosphere.2022.133900 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001765.pica (DE-627)ELV057029105 (ELSEVIER)S0045-6535(22)00393-9 DE-627 ger DE-627 rakwb eng 004 620 VZ 54.25 bkl Santibáñez-Andrade, Miguel verfasserin aut Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. SETD2 Elsevier PM10 Elsevier A549 Elsevier Aneuploidy Elsevier Chromosomal instability Elsevier Mitotic spindle Elsevier Sánchez-Pérez, Yesennia oth Chirino, Yolanda I. oth Morales-Bárcenas, Rocío oth Quintana-Belmares, Raúl oth García-Cuellar, Claudia M. oth Enthalten in Elsevier Science Shterenlikht, Anton ELSEVIER MPI vs Fortran coarrays beyond 100k cores: 3D cellular automata 2019 chemistry, biology and toxicology as related to environmental problems Amsterdam [u.a.] (DE-627)ELV002112701 volume:295 year:2022 pages:0 https://doi.org/10.1016/j.chemosphere.2022.133900 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.25 Parallele Datenverarbeitung VZ AR 295 2022 0 |
| spelling |
10.1016/j.chemosphere.2022.133900 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001765.pica (DE-627)ELV057029105 (ELSEVIER)S0045-6535(22)00393-9 DE-627 ger DE-627 rakwb eng 004 620 VZ 54.25 bkl Santibáñez-Andrade, Miguel verfasserin aut Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. SETD2 Elsevier PM10 Elsevier A549 Elsevier Aneuploidy Elsevier Chromosomal instability Elsevier Mitotic spindle Elsevier Sánchez-Pérez, Yesennia oth Chirino, Yolanda I. oth Morales-Bárcenas, Rocío oth Quintana-Belmares, Raúl oth García-Cuellar, Claudia M. oth Enthalten in Elsevier Science Shterenlikht, Anton ELSEVIER MPI vs Fortran coarrays beyond 100k cores: 3D cellular automata 2019 chemistry, biology and toxicology as related to environmental problems Amsterdam [u.a.] (DE-627)ELV002112701 volume:295 year:2022 pages:0 https://doi.org/10.1016/j.chemosphere.2022.133900 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.25 Parallele Datenverarbeitung VZ AR 295 2022 0 |
| allfields_unstemmed |
10.1016/j.chemosphere.2022.133900 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001765.pica (DE-627)ELV057029105 (ELSEVIER)S0045-6535(22)00393-9 DE-627 ger DE-627 rakwb eng 004 620 VZ 54.25 bkl Santibáñez-Andrade, Miguel verfasserin aut Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. SETD2 Elsevier PM10 Elsevier A549 Elsevier Aneuploidy Elsevier Chromosomal instability Elsevier Mitotic spindle Elsevier Sánchez-Pérez, Yesennia oth Chirino, Yolanda I. oth Morales-Bárcenas, Rocío oth Quintana-Belmares, Raúl oth García-Cuellar, Claudia M. oth Enthalten in Elsevier Science Shterenlikht, Anton ELSEVIER MPI vs Fortran coarrays beyond 100k cores: 3D cellular automata 2019 chemistry, biology and toxicology as related to environmental problems Amsterdam [u.a.] (DE-627)ELV002112701 volume:295 year:2022 pages:0 https://doi.org/10.1016/j.chemosphere.2022.133900 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.25 Parallele Datenverarbeitung VZ AR 295 2022 0 |
| allfieldsGer |
10.1016/j.chemosphere.2022.133900 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001765.pica (DE-627)ELV057029105 (ELSEVIER)S0045-6535(22)00393-9 DE-627 ger DE-627 rakwb eng 004 620 VZ 54.25 bkl Santibáñez-Andrade, Miguel verfasserin aut Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. SETD2 Elsevier PM10 Elsevier A549 Elsevier Aneuploidy Elsevier Chromosomal instability Elsevier Mitotic spindle Elsevier Sánchez-Pérez, Yesennia oth Chirino, Yolanda I. oth Morales-Bárcenas, Rocío oth Quintana-Belmares, Raúl oth García-Cuellar, Claudia M. oth Enthalten in Elsevier Science Shterenlikht, Anton ELSEVIER MPI vs Fortran coarrays beyond 100k cores: 3D cellular automata 2019 chemistry, biology and toxicology as related to environmental problems Amsterdam [u.a.] (DE-627)ELV002112701 volume:295 year:2022 pages:0 https://doi.org/10.1016/j.chemosphere.2022.133900 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 54.25 Parallele Datenverarbeitung VZ AR 295 2022 0 |
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10.1016/j.chemosphere.2022.133900 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001765.pica (DE-627)ELV057029105 (ELSEVIER)S0045-6535(22)00393-9 DE-627 ger DE-627 rakwb eng 004 620 VZ 54.25 bkl Santibáñez-Andrade, Miguel verfasserin aut Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. 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Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells |
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Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. |
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Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. |
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Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV057029105</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626044404.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">220808s2022 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.chemosphere.2022.133900</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001765.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV057029105</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0045-6535(22)00393-9</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">004</subfield><subfield code="a">620</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">54.25</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Santibáñez-Andrade, Miguel</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Particulate matter (PM10) destabilizes mitotic spindle through downregulation of SETD2 in A549 lung cancer cells</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022transfer abstract</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Air pollution represents an environmental problem, impacting negatively in human health. Particulate matter of 10 μm or less in diameter (PM10) is related to pulmonary diseases, including lung cancer. Mitotic spindle is made up by chromosome-microtubule (MT) interactions, where SETD2 plays an important role in MT stability. SETD2 binds and activates α-TUBULIN sub-unit and promotes MT polymerization. Alongside this mechanism, the spindle assembly checkpoint (SAC) senses the adequate mitotic progression through proteins such as BUBR1, AURORA B and SURVIVIN. Alterations in MT dynamics as well as in SAC cause aneuploidy and chromosomal instability, a common phenotype in cancer cells. In this study, we evaluated the effect of PM10 in the expression and protein levels of SETD2, as well as the effect in the expression and protein levels of SAC and mitotic components involved in chromosomal segregation/mitosis, using the A549 lung cancer cell line. A549 cell cultures were exposed to PM10 (10 μg/cm2) for 24 h to evaluate the expression and protein levels of SETD2 (SETD2), TUBA1A (α-TUBULIN), CCNB1 (CYCLIN B1), BUB1B (BUBR1), AURKB (AURORA B) and BIRC5 (SURVIVIN). We observed that PM10 decreases the expression and protein levels of SETD2, α-TUBULIN and BUBR1 and increases the levels of AURORA B and SURVIVIN in A549 cells, compared with non-treated cells. PM10 also caused a decrease in mitotic index and in the percentage of cells in G2/M when compared with control group. Co-localization of SETD2/α -TUB was lower in PM10-treated cells in comparison with non-treated cells. Finally, micronuclei (MN) frequency was higher in PM10-treated cells in contrast with non-treated cells, being whole chromosomes more common in PM10-treated MN than in non-treated MN. Our results suggest that PM10 causes missegregation and aneuploidy through downregulation of SETD2 and SAC components, inducing aneuploidy and predisposing to the generation of chromosomal instability in transformed cells.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">SETD2</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">PM10</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">A549</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Aneuploidy</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Chromosomal instability</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Mitotic spindle</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sánchez-Pérez, Yesennia</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chirino, Yolanda I.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Morales-Bárcenas, Rocío</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Quintana-Belmares, Raúl</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">García-Cuellar, Claudia M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Shterenlikht, Anton ELSEVIER</subfield><subfield code="t">MPI vs Fortran coarrays beyond 100k cores: 3D cellular automata</subfield><subfield code="d">2019</subfield><subfield code="d">chemistry, biology and toxicology as related to environmental problems</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV002112701</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:295</subfield><subfield code="g">year:2022</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.chemosphere.2022.133900</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">54.25</subfield><subfield code="j">Parallele Datenverarbeitung</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">295</subfield><subfield code="j">2022</subfield><subfield code="h">0</subfield></datafield></record></collection>
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