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Knockdown EIF3C Suppresses Cell Proliferation and Increases Apoptosis in Pancreatic Cancer Cell.
Jiao, Heng; Zeng, Lingxiao; Yang, Shengsheng; Zhang, Jianpeng; Lou, Wenhui.
Afiliación
  • Jiao H; Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
  • Zeng L; Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
  • Yang S; Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Second Military Medical University, Shanghai, China.
  • Zhang J; Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Second Military Medical University, Shanghai, China.
  • Lou W; Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Dose Response ; 18(3): 1559325820950061, 2020.
Article en En | MEDLINE | ID: mdl-32973416
ABSTRACT
Increasing evidence shows that eukaryotic initiation factor subunit (EIF3C) plays a crucial role in development of tumors. However, the underlying roles of EIF3Cin the development of pancreatic cancer (PC) remain unknown. In this study, we examined the expression of EIF3C in PC tissues, their adjacent normal tissues and 3 cell lines (SW1990, PANC-1 and AsPC-1). Moreover, the EIF3C-shRNA lentivirus was constructed to suppress EIF3C expression. Following this, the cell colony formation assay was employed to evaluate proliferation ability of PC cells. Meanwhile, the cell cycle and apoptotic assays were also performed by flow cytometry. We found that level of EIF3C in PC tissues was significantly increased compared with that in adjacent normal tissues. Furthermore, the knockdown of EIF3C can significantly reduce cell proliferation, block cell cycle in G2/M and induce apoptosis in both SW1990 and PANC-1 cells. Our findings suggest that EIF3C plays a crucial role in the progression of PC and may be a potential target in the treatment of PC.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Dose Response Año: 2020 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Dose Response Año: 2020 Tipo del documento: Article País de afiliación: China