Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines

Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further e...
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Autor*in:	Palumbo, Paola [verfasserIn] Lombardi, Francesca [verfasserIn] Augello, Francesca Rosaria [verfasserIn] Giusti, Ilaria [verfasserIn] Dolo, Vincenza [verfasserIn] Leocata, Pietro [verfasserIn] Cifone, Maria Grazia [verfasserIn] Cinque, Benedetta [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Glioblastoma U87MG T98G Glioma stem cells Inflammation COX-2 COX-2 inhibitor NS398 Autophagy Extracellular vesicles

Übergeordnetes Werk:	Enthalten in: Cancer cell international - London : BioMed Central, 2001, 20(2020), 1 vom: 13. Mai
Übergeordnetes Werk:	volume:20 ; year:2020 ; number:1 ; day:13 ; month:05

Links:	Volltext

DOI / URN:	10.1186/s12935-020-01250-7

Katalog-ID:	SPR039697762

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520			\|a Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology.
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allfields	10.1186/s12935-020-01250-7 doi (DE-627)SPR039697762 (SPR)s12935-020-01250-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Palumbo, Paola verfasserin aut Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology. Glioblastoma (dpeaa)DE-He213 U87MG (dpeaa)DE-He213 T98G (dpeaa)DE-He213 Glioma stem cells (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 COX-2 (dpeaa)DE-He213 COX-2 inhibitor (dpeaa)DE-He213 NS398 (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Extracellular vesicles (dpeaa)DE-He213 Lombardi, Francesca verfasserin aut Augello, Francesca Rosaria verfasserin aut Giusti, Ilaria verfasserin aut Dolo, Vincenza verfasserin aut Leocata, Pietro verfasserin aut Cifone, Maria Grazia verfasserin aut Cinque, Benedetta verfasserin aut Enthalten in Cancer cell international London : BioMed Central, 2001 20(2020), 1 vom: 13. Mai (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:20 year:2020 number:1 day:13 month:05 https://dx.doi.org/10.1186/s12935-020-01250-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 20 2020 1 13 05
spelling	10.1186/s12935-020-01250-7 doi (DE-627)SPR039697762 (SPR)s12935-020-01250-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Palumbo, Paola verfasserin aut Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology. Glioblastoma (dpeaa)DE-He213 U87MG (dpeaa)DE-He213 T98G (dpeaa)DE-He213 Glioma stem cells (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 COX-2 (dpeaa)DE-He213 COX-2 inhibitor (dpeaa)DE-He213 NS398 (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Extracellular vesicles (dpeaa)DE-He213 Lombardi, Francesca verfasserin aut Augello, Francesca Rosaria verfasserin aut Giusti, Ilaria verfasserin aut Dolo, Vincenza verfasserin aut Leocata, Pietro verfasserin aut Cifone, Maria Grazia verfasserin aut Cinque, Benedetta verfasserin aut Enthalten in Cancer cell international London : BioMed Central, 2001 20(2020), 1 vom: 13. Mai (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:20 year:2020 number:1 day:13 month:05 https://dx.doi.org/10.1186/s12935-020-01250-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 20 2020 1 13 05
allfields_unstemmed	10.1186/s12935-020-01250-7 doi (DE-627)SPR039697762 (SPR)s12935-020-01250-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Palumbo, Paola verfasserin aut Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology. Glioblastoma (dpeaa)DE-He213 U87MG (dpeaa)DE-He213 T98G (dpeaa)DE-He213 Glioma stem cells (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 COX-2 (dpeaa)DE-He213 COX-2 inhibitor (dpeaa)DE-He213 NS398 (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Extracellular vesicles (dpeaa)DE-He213 Lombardi, Francesca verfasserin aut Augello, Francesca Rosaria verfasserin aut Giusti, Ilaria verfasserin aut Dolo, Vincenza verfasserin aut Leocata, Pietro verfasserin aut Cifone, Maria Grazia verfasserin aut Cinque, Benedetta verfasserin aut Enthalten in Cancer cell international London : BioMed Central, 2001 20(2020), 1 vom: 13. Mai (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:20 year:2020 number:1 day:13 month:05 https://dx.doi.org/10.1186/s12935-020-01250-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 20 2020 1 13 05
allfieldsGer	10.1186/s12935-020-01250-7 doi (DE-627)SPR039697762 (SPR)s12935-020-01250-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Palumbo, Paola verfasserin aut Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology. Glioblastoma (dpeaa)DE-He213 U87MG (dpeaa)DE-He213 T98G (dpeaa)DE-He213 Glioma stem cells (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 COX-2 (dpeaa)DE-He213 COX-2 inhibitor (dpeaa)DE-He213 NS398 (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Extracellular vesicles (dpeaa)DE-He213 Lombardi, Francesca verfasserin aut Augello, Francesca Rosaria verfasserin aut Giusti, Ilaria verfasserin aut Dolo, Vincenza verfasserin aut Leocata, Pietro verfasserin aut Cifone, Maria Grazia verfasserin aut Cinque, Benedetta verfasserin aut Enthalten in Cancer cell international London : BioMed Central, 2001 20(2020), 1 vom: 13. Mai (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:20 year:2020 number:1 day:13 month:05 https://dx.doi.org/10.1186/s12935-020-01250-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 20 2020 1 13 05
allfieldsSound	10.1186/s12935-020-01250-7 doi (DE-627)SPR039697762 (SPR)s12935-020-01250-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Palumbo, Paola verfasserin aut Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology. Glioblastoma (dpeaa)DE-He213 U87MG (dpeaa)DE-He213 T98G (dpeaa)DE-He213 Glioma stem cells (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 COX-2 (dpeaa)DE-He213 COX-2 inhibitor (dpeaa)DE-He213 NS398 (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Extracellular vesicles (dpeaa)DE-He213 Lombardi, Francesca verfasserin aut Augello, Francesca Rosaria verfasserin aut Giusti, Ilaria verfasserin aut Dolo, Vincenza verfasserin aut Leocata, Pietro verfasserin aut Cifone, Maria Grazia verfasserin aut Cinque, Benedetta verfasserin aut Enthalten in Cancer cell international London : BioMed Central, 2001 20(2020), 1 vom: 13. Mai (DE-627)355989204 (DE-600)2091573-1 1475-2867 nnns volume:20 year:2020 number:1 day:13 month:05 https://dx.doi.org/10.1186/s12935-020-01250-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 20 2020 1 13 05
language	English
source	Enthalten in Cancer cell international 20(2020), 1 vom: 13. Mai volume:20 year:2020 number:1 day:13 month:05
sourceStr	Enthalten in Cancer cell international 20(2020), 1 vom: 13. Mai volume:20 year:2020 number:1 day:13 month:05
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Glioblastoma U87MG T98G Glioma stem cells Inflammation COX-2 COX-2 inhibitor NS398 Autophagy Extracellular vesicles
dewey-raw	610
isfreeaccess_bool	true
container_title	Cancer cell international
authorswithroles_txt_mv	Palumbo, Paola @@aut@@ Lombardi, Francesca @@aut@@ Augello, Francesca Rosaria @@aut@@ Giusti, Ilaria @@aut@@ Dolo, Vincenza @@aut@@ Leocata, Pietro @@aut@@ Cifone, Maria Grazia @@aut@@ Cinque, Benedetta @@aut@@
publishDateDaySort_date	2020-05-13T00:00:00Z
hierarchy_top_id	355989204
dewey-sort	3610
id	SPR039697762
language_de	englisch
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The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. 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author	Palumbo, Paola
spellingShingle	Palumbo, Paola ddc 610 bkl 44.00 misc Glioblastoma misc U87MG misc T98G misc Glioma stem cells misc Inflammation misc COX-2 misc COX-2 inhibitor misc NS398 misc Autophagy misc Extracellular vesicles Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines
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topic_title	610 ASE 44.00 bkl Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines Glioblastoma (dpeaa)DE-He213 U87MG (dpeaa)DE-He213 T98G (dpeaa)DE-He213 Glioma stem cells (dpeaa)DE-He213 Inflammation (dpeaa)DE-He213 COX-2 (dpeaa)DE-He213 COX-2 inhibitor (dpeaa)DE-He213 NS398 (dpeaa)DE-He213 Autophagy (dpeaa)DE-He213 Extracellular vesicles (dpeaa)DE-He213
topic	ddc 610 bkl 44.00 misc Glioblastoma misc U87MG misc T98G misc Glioma stem cells misc Inflammation misc COX-2 misc COX-2 inhibitor misc NS398 misc Autophagy misc Extracellular vesicles
topic_unstemmed	ddc 610 bkl 44.00 misc Glioblastoma misc U87MG misc T98G misc Glioma stem cells misc Inflammation misc COX-2 misc COX-2 inhibitor misc NS398 misc Autophagy misc Extracellular vesicles
topic_browse	ddc 610 bkl 44.00 misc Glioblastoma misc U87MG misc T98G misc Glioma stem cells misc Inflammation misc COX-2 misc COX-2 inhibitor misc NS398 misc Autophagy misc Extracellular vesicles
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title	Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines
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title_full	Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines
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author_browse	Palumbo, Paola Lombardi, Francesca Augello, Francesca Rosaria Giusti, Ilaria Dolo, Vincenza Leocata, Pietro Cifone, Maria Grazia Cinque, Benedetta
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title_sort	biological effects of selective cox-2 inhibitor ns398 on human glioblastoma cell lines
title_auth	Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines
abstract	Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology.
abstractGer	Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology.
abstract_unstemmed	Background Cyclooxygenase-2 (COX-2), an inflammation-associated enzyme, has been implicated in tumorigenesis and progression of glioblastoma (GBM). The poor survival of GBM was mainly associated with the presence of glioma stem cells (GSC) and the markedly inflammatory microenvironment. To further explore the involvement of COX-2 in glioma biology, the effects of NS398, a selective COX-2 inhibitor, were evaluated on GSC derived from COX-2 expressing GBM cell lines, i.e., U87MG and T98G, in terms of neurospheres’ growth, autophagy, and extracellular vesicle (EV) release. Methods Neurospheres’ growth and morphology were evaluated by optical and scanning electron microscopy. Autophagy was measured by staining acidic vesicular organelles. Extracellular vesicles (EV), released from neurospheres, were analyzed by transmission electron microscopy. The autophagic proteins Beclin-1 and LC3B, as well as the EV markers CD63 and CD81, were analyzed by western blotting. The scratch assay test was used to evaluate the NS398 influence on GBM cell migration. Results Both cell lines were strongly influenced by NS398 exposure, as showed by morphological changes, reduced growth rate, and appearance of autophagy. Furthermore, the inhibitor led to a functional change of EV released by neurospheres. Indeed, EV secreted by NS398-treated GSC, but not those from control cells, were able to significantly inhibit adherent U87MG and T98G cell migration and induced autophagy in recipient cells, thus leading to effects quite similar to those directly caused by NS398 in the same cells. Conclusion Despite the intrinsic diversity and individual genetic features of U87MG and T98G, comparable effects were exerted by the COX-2 inhibitor NS398 on both GBM cell lines. Overall, our findings support the crucial role of the inflammatory-associated COX-2/PGE2 system in glioma and glioma stem cell biology.
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title_short	Biological effects of selective COX-2 inhibitor NS398 on human glioblastoma cell lines
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author2	Lombardi, Francesca Augello, Francesca Rosaria Giusti, Ilaria Dolo, Vincenza Leocata, Pietro Cifone, Maria Grazia Cinque, Benedetta
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