The effects of miRNAs-107 on cell proliferation, senescence and invasion of pancreatic cancer PANC-1 cells
10.3760/cma.j.issn.1007-8118.2017.12.012
- VernacularTitle:微RNAs-107对胰腺癌PANC-1细胞增殖、衰老和侵袭的影响
- Author:
Jungang ZHANG
1
;
Weiding WU
;
Yuhua ZHANG
;
Ying SHI
;
Zhiming HU
;
Chengwu ZHANG
;
Dongsheng HUANG
;
Defei HONG
Author Information
1. 310014,杭州医学院附属人民医院肝胆胰外科
- Keywords:
Pancreatic cancer;
MiRNAs-107(MiR-107);
Proliferation;
Senescence;
Invasion
- From:
Chinese Journal of Hepatobiliary Surgery
2017;23(12):836-840
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of miRNAs-107 (miR-107) on pancreatic cancer proliferation,senescence and invasion.Methods MiR-107 expression levels in 3 pancreatic cancer cell lines PANC-1,ASPC-1,BXPC-3 and normal pancreatic HTERT-HPNE cells were studied by quantitative reverse transcription-polymerase chain reaction (qRT-PCR).PANC-1 cells were transfected with 50 nmol/L anti-miR-107 or negative control using Lipofectamine 2000.After transfection,the miR-107 expression was measured by qRT-PCR.Cell proliferation was tested by methylthiazol tetrazolium (MTT) assay.Cell senescence was detected by β-galactosidase staining.The expression levels of PCNA,P16INK4A and MMP2 were measured by qRT-PCR.Results Compared with the HTERT-HPNE cells,the expression level of miR-107 in 3 pancreatic cancer cell lines was significantly increased (P < 0.01).After transfected with 50 nmol/L anti-miR-107,cell proliferation was inhibited,and cell senescence were increased in PANC-1 cells (P < 0.05),and there was no obvious change in cell invasion.Compared with the HTERT-HPNE cells,after transfected with anti-miR-107,the PCNA expression was significantly decreased and P16INK4A was significantly increased,but expression of M MP2 didn't change significantly.Conclusions These results demonstrate that miR-107 promotes the proliferation and escapes cell senescence in PANC-1 cells by targeting PCNA and P16INK4A.But it has no obvious effects on cell invasion.Therefore,it may be a new target for the biologic therapy for pancreatic cancer.