Methyl-CpG-binding domain 3 inhibits stemness of pancreatic cancer cells via Hippo signaling
Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, s...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wang, Huizhi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020transfer abstract |
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| Schlagwörter: |
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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:393 ; year:2020 ; number:1 ; day:1 ; month:08 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.yexcr.2020.112091 |
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ELV050535714 |
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| 245 | 1 | 0 | |a Methyl-CpG-binding domain 3 inhibits stemness of pancreatic cancer cells via Hippo signaling |
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| 520 | |a Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. | ||
| 520 | |a Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. | ||
| 650 | 7 | |a MBD3 |2 Elsevier | |
| 650 | 7 | |a Stemness |2 Elsevier | |
| 650 | 7 | |a Hippo signaling |2 Elsevier | |
| 650 | 7 | |a Pancreatic cancer |2 Elsevier | |
| 650 | 7 | |a Proliferation |2 Elsevier | |
| 700 | 1 | |a Feng, Wen |4 oth | |
| 700 | 1 | |a Chen, Wei |4 oth | |
| 700 | 1 | |a He, Junbo |4 oth | |
| 700 | 1 | |a Min, Jingyu |4 oth | |
| 700 | 1 | |a Liu, Yawen |4 oth | |
| 700 | 1 | |a Li, Feifan |4 oth | |
| 700 | 1 | |a Chen, Jiaxi |4 oth | |
| 700 | 1 | |a Wu, Shuhui |4 oth | |
| 700 | 1 | |a Chen, Baoding |4 oth | |
| 700 | 1 | |a Gong, Aihua |4 oth | |
| 700 | 1 | |a Xu, Min |4 oth | |
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10.1016/j.yexcr.2020.112091 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001029.pica (DE-627)ELV050535714 (ELSEVIER)S0014-4827(20)30334-7 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Wang, Huizhi verfasserin aut Methyl-CpG-binding domain 3 inhibits stemness of pancreatic cancer cells via Hippo signaling 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. MBD3 Elsevier Stemness Elsevier Hippo signaling Elsevier Pancreatic cancer Elsevier Proliferation Elsevier Feng, Wen oth Chen, Wei oth He, Junbo oth Min, Jingyu oth Liu, Yawen oth Li, Feifan oth Chen, Jiaxi oth Wu, Shuhui oth Chen, Baoding oth Gong, Aihua oth Xu, Min 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:393 year:2020 number:1 day:1 month:08 pages:0 https://doi.org/10.1016/j.yexcr.2020.112091 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 393 2020 1 1 0801 0 |
| spelling |
10.1016/j.yexcr.2020.112091 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001029.pica (DE-627)ELV050535714 (ELSEVIER)S0014-4827(20)30334-7 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Wang, Huizhi verfasserin aut Methyl-CpG-binding domain 3 inhibits stemness of pancreatic cancer cells via Hippo signaling 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. MBD3 Elsevier Stemness Elsevier Hippo signaling Elsevier Pancreatic cancer Elsevier Proliferation Elsevier Feng, Wen oth Chen, Wei oth He, Junbo oth Min, Jingyu oth Liu, Yawen oth Li, Feifan oth Chen, Jiaxi oth Wu, Shuhui oth Chen, Baoding oth Gong, Aihua oth Xu, Min 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:393 year:2020 number:1 day:1 month:08 pages:0 https://doi.org/10.1016/j.yexcr.2020.112091 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 393 2020 1 1 0801 0 |
| allfields_unstemmed |
10.1016/j.yexcr.2020.112091 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001029.pica (DE-627)ELV050535714 (ELSEVIER)S0014-4827(20)30334-7 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Wang, Huizhi verfasserin aut Methyl-CpG-binding domain 3 inhibits stemness of pancreatic cancer cells via Hippo signaling 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. MBD3 Elsevier Stemness Elsevier Hippo signaling Elsevier Pancreatic cancer Elsevier Proliferation Elsevier Feng, Wen oth Chen, Wei oth He, Junbo oth Min, Jingyu oth Liu, Yawen oth Li, Feifan oth Chen, Jiaxi oth Wu, Shuhui oth Chen, Baoding oth Gong, Aihua oth Xu, Min 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:393 year:2020 number:1 day:1 month:08 pages:0 https://doi.org/10.1016/j.yexcr.2020.112091 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 393 2020 1 1 0801 0 |
| allfieldsGer |
10.1016/j.yexcr.2020.112091 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001029.pica (DE-627)ELV050535714 (ELSEVIER)S0014-4827(20)30334-7 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Wang, Huizhi verfasserin aut Methyl-CpG-binding domain 3 inhibits stemness of pancreatic cancer cells via Hippo signaling 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. MBD3 Elsevier Stemness Elsevier Hippo signaling Elsevier Pancreatic cancer Elsevier Proliferation Elsevier Feng, Wen oth Chen, Wei oth He, Junbo oth Min, Jingyu oth Liu, Yawen oth Li, Feifan oth Chen, Jiaxi oth Wu, Shuhui oth Chen, Baoding oth Gong, Aihua oth Xu, Min 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:393 year:2020 number:1 day:1 month:08 pages:0 https://doi.org/10.1016/j.yexcr.2020.112091 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 393 2020 1 1 0801 0 |
| allfieldsSound |
10.1016/j.yexcr.2020.112091 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001029.pica (DE-627)ELV050535714 (ELSEVIER)S0014-4827(20)30334-7 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.44 bkl Wang, Huizhi verfasserin aut Methyl-CpG-binding domain 3 inhibits stemness of pancreatic cancer cells via Hippo signaling 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. MBD3 Elsevier Stemness Elsevier Hippo signaling Elsevier Pancreatic cancer Elsevier Proliferation Elsevier Feng, Wen oth Chen, Wei oth He, Junbo oth Min, Jingyu oth Liu, Yawen oth Li, Feifan oth Chen, Jiaxi oth Wu, Shuhui oth Chen, Baoding oth Gong, Aihua oth Xu, Min 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:393 year:2020 number:1 day:1 month:08 pages:0 https://doi.org/10.1016/j.yexcr.2020.112091 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 393 2020 1 1 0801 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:393 year:2020 number:1 day:1 month:08 pages:0 |
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Wang, Huizhi @@aut@@ Feng, Wen @@oth@@ Chen, Wei @@oth@@ He, Junbo @@oth@@ Min, Jingyu @@oth@@ Liu, Yawen @@oth@@ Li, Feifan @@oth@@ Chen, Jiaxi @@oth@@ Wu, Shuhui @@oth@@ Chen, Baoding @@oth@@ Gong, Aihua @@oth@@ Xu, Min @@oth@@ |
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methyl-cpg-binding domain 3 inhibits stemness of pancreatic cancer cells via hippo signaling |
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Methyl-CpG-binding domain 3 inhibits stemness of pancreatic cancer cells via Hippo signaling |
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Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. |
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Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. |
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Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer. |
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Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Methyl-CpG-binding domain 3 (MBD3), as an induced stem cells reprogramming barrier, has an abnormal expression in various prevalent malignancies. However, in pancreatic cancer cell stemness, the roles of MBD3 remain unclear. In our study, the effects of MBD3 were investigated on the proliferation, stemness and the underlying mechanism in pancreatic cancer cells. Firstly, MBD3 knockdown was proved to promote proliferation and sphere formation of pancreatic cancer cells and tumorigenesis, while MBD3 upregulation inhibited the above results. Also, MBD3 downregulation notably increased stemness markers level of OCT4, NANOG and SOX2, and MBD3 upregulation resulted in the opposite effects. Mechanically, it was found that MBD3 involved in activation of Hippo pathway. There was a negative correlation between MBD3 and YAP expression in TCGA database. MBD3 knockdown improved YAP expression, and promoted YAP nuclear translocation increased TEAD luciferase activity, while MBD3 overexpression reversed the above results. Further evidence revealed that YAP could bind to MBD3, and decreased MBD3 expression. Collectively, MBD3 bound to YAP to significantly inhibit proliferation and weaken stemness maintenance in pancreatic cancer cells, as well as reduce tumorigenesis via Hippo signaling. Thus, MBD3 may serve as a potential molecular biomarker for exploring new therapeutic strategies to treat pancreatic cancer.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">MBD3</subfield><subfield code="2">Elsevier</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">Hippo signaling</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Pancreatic cancer</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Proliferation</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Feng, Wen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Wei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Junbo</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Min, Jingyu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Yawen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Feifan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Jiaxi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wu, Shuhui</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Baoding</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gong, Aihua</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xu, Min</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:393</subfield><subfield code="g">year:2020</subfield><subfield code="g">number:1</subfield><subfield code="g">day:1</subfield><subfield code="g">month:08</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.2020.112091</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">393</subfield><subfield code="j">2020</subfield><subfield code="e">1</subfield><subfield code="b">1</subfield><subfield code="c">0801</subfield><subfield code="h">0</subfield></datafield></record></collection>
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