miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L
Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stem...
Ausführliche Beschreibung
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| Autor*in: |
Lv, Lv [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS - 2012, ECR, Orlando, Fla |
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| Übergeordnetes Werk: |
volume:385 ; year:2019 ; number:1 ; day:1 ; month:12 ; pages:0 |
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| DOI / URN: |
10.1016/j.yexcr.2019.111597 |
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| 245 | 1 | 0 | |a miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L |
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| 520 | |a Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. | ||
| 520 | |a Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. | ||
| 650 | 7 | |a Stemness |2 Elsevier | |
| 650 | 7 | |a miR-133b |2 Elsevier | |
| 650 | 7 | |a Colorectal cancer |2 Elsevier | |
| 650 | 7 | |a Chemoresistance |2 Elsevier | |
| 650 | 7 | |a DOT1L |2 Elsevier | |
| 650 | 7 | |a H3K79me2 |2 Elsevier | |
| 700 | 1 | |a Li, Qiang |4 oth | |
| 700 | 1 | |a Chen, Shaohua |4 oth | |
| 700 | 1 | |a Zhang, Xuemei |4 oth | |
| 700 | 1 | |a Tao, Xuan |4 oth | |
| 700 | 1 | |a Tang, Xianmin |4 oth | |
| 700 | 1 | |a Wang, Shengtao |4 oth | |
| 700 | 1 | |a Che, Guosong |4 oth | |
| 700 | 1 | |a Yu, Yaqun |4 oth | |
| 700 | 1 | |a He, Liang |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Academic Press |t 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |d 2012 |d ECR |g Orlando, Fla |w (DE-627)ELV011050691 |
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10.1016/j.yexcr.2019.111597 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000961.pica (DE-627)ELV04833569X (ELSEVIER)S0014-4827(19)30454-9 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Lv, Lv verfasserin aut miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Stemness Elsevier miR-133b Elsevier Colorectal cancer Elsevier Chemoresistance Elsevier DOT1L Elsevier H3K79me2 Elsevier Li, Qiang oth Chen, Shaohua oth Zhang, Xuemei oth Tao, Xuan oth Tang, Xianmin oth Wang, Shengtao oth Che, Guosong oth Yu, Yaqun oth He, Liang oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:385 year:2019 number:1 day:1 month:12 pages:0 https://doi.org/10.1016/j.yexcr.2019.111597 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 385 2019 1 1 1201 0 |
| spelling |
10.1016/j.yexcr.2019.111597 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000961.pica (DE-627)ELV04833569X (ELSEVIER)S0014-4827(19)30454-9 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Lv, Lv verfasserin aut miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Stemness Elsevier miR-133b Elsevier Colorectal cancer Elsevier Chemoresistance Elsevier DOT1L Elsevier H3K79me2 Elsevier Li, Qiang oth Chen, Shaohua oth Zhang, Xuemei oth Tao, Xuan oth Tang, Xianmin oth Wang, Shengtao oth Che, Guosong oth Yu, Yaqun oth He, Liang oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:385 year:2019 number:1 day:1 month:12 pages:0 https://doi.org/10.1016/j.yexcr.2019.111597 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 385 2019 1 1 1201 0 |
| allfields_unstemmed |
10.1016/j.yexcr.2019.111597 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000961.pica (DE-627)ELV04833569X (ELSEVIER)S0014-4827(19)30454-9 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Lv, Lv verfasserin aut miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Stemness Elsevier miR-133b Elsevier Colorectal cancer Elsevier Chemoresistance Elsevier DOT1L Elsevier H3K79me2 Elsevier Li, Qiang oth Chen, Shaohua oth Zhang, Xuemei oth Tao, Xuan oth Tang, Xianmin oth Wang, Shengtao oth Che, Guosong oth Yu, Yaqun oth He, Liang oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:385 year:2019 number:1 day:1 month:12 pages:0 https://doi.org/10.1016/j.yexcr.2019.111597 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 385 2019 1 1 1201 0 |
| allfieldsGer |
10.1016/j.yexcr.2019.111597 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000961.pica (DE-627)ELV04833569X (ELSEVIER)S0014-4827(19)30454-9 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Lv, Lv verfasserin aut miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Stemness Elsevier miR-133b Elsevier Colorectal cancer Elsevier Chemoresistance Elsevier DOT1L Elsevier H3K79me2 Elsevier Li, Qiang oth Chen, Shaohua oth Zhang, Xuemei oth Tao, Xuan oth Tang, Xianmin oth Wang, Shengtao oth Che, Guosong oth Yu, Yaqun oth He, Liang oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:385 year:2019 number:1 day:1 month:12 pages:0 https://doi.org/10.1016/j.yexcr.2019.111597 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 385 2019 1 1 1201 0 |
| allfieldsSound |
10.1016/j.yexcr.2019.111597 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000000961.pica (DE-627)ELV04833569X (ELSEVIER)S0014-4827(19)30454-9 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Lv, Lv verfasserin aut miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L 2019transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. Stemness Elsevier miR-133b Elsevier Colorectal cancer Elsevier Chemoresistance Elsevier DOT1L Elsevier H3K79me2 Elsevier Li, Qiang oth Chen, Shaohua oth Zhang, Xuemei oth Tao, Xuan oth Tang, Xianmin oth Wang, Shengtao oth Che, Guosong oth Yu, Yaqun oth He, Liang oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:385 year:2019 number:1 day:1 month:12 pages:0 https://doi.org/10.1016/j.yexcr.2019.111597 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 385 2019 1 1 1201 0 |
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Enthalten in 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS Orlando, Fla volume:385 year:2019 number:1 day:1 month:12 pages:0 |
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mir-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase dot1l |
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miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L |
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Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. |
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Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. |
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Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance. |
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More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Cancer stem cells (CSCs) are a subpopulation of chemoresistant cells that play a critical role in disease recurrence following chemotherapy. It has been reported that microRNA-133b (miR-133b) acts as a tumor suppressor in colorectal cancer (CRC). However, whether miR-133b is associated with CRC stemness and chemoresistance is not clear. In this study, we report that miR-133b is downregulated in colorectal spheroids, which are enriched with CSCs and display stem cell-like characteristics, including upreulation of CSCs surface markers and elevated chemoresistance. Additionally, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP), indicating a negative role of miR-133b in regulating CRC stemness and chemoresistance. Moreover, miR-133b directly targets and suppresses the expression of disruptor of telomeric silencing 1-like (DOT1L), an exclusive H3K79 methyltransferase. Furthermore, miR-133b overexpression suppresses DOT1L-mediated H3K79me2 modification of stem cell genes, which is consistent with their downregulated transcription. More importantly, DOT1L restoration abrogates the suppressive effects of miR-133b on CRC stemness and chemoresistance, hence demonstrating that miR-133b regulates CRC stemness and chemoresistance through targeting DOT1L. Overall, these results imply that miR-133b might represent a novel therapeutic target in interfering CRC stemness and chemoresistance.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Stemness</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">miR-133b</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Colorectal cancer</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Chemoresistance</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">DOT1L</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">H3K79me2</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Qiang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Shaohua</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Xuemei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tao, Xuan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tang, Xianmin</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Shengtao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Che, Guosong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yu, Yaqun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Liang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="t">72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS</subfield><subfield code="d">2012</subfield><subfield code="d">ECR</subfield><subfield code="g">Orlando, Fla</subfield><subfield code="w">(DE-627)ELV011050691</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:385</subfield><subfield code="g">year:2019</subfield><subfield code="g">number:1</subfield><subfield code="g">day:1</subfield><subfield code="g">month:12</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.yexcr.2019.111597</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="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.44</subfield><subfield code="j">Parasitologie</subfield><subfield code="x">Medizin</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">385</subfield><subfield code="j">2019</subfield><subfield code="e">1</subfield><subfield code="b">1</subfield><subfield code="c">1201</subfield><subfield code="h">0</subfield></datafield></record></collection>
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