Effects of miR-125a-5p on Cell Proliferation,Apoptosis and Cell Cycle of Pancreatic Cancer Cells.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao
; 38(4): 415-21, 2016 Aug.
Article
in En
| MEDLINE
| ID: mdl-27594154
Objective To investigate the effects of miR-125a-5p on cell proliferation,apoptosis and cell cycle of pancreatic cancer cells.Methods The expression level of miR-125a-5p in pancreatic cancer was determined using quantitative real-time polymerase chain reaction analysis in 4 pairs of pancreatic cancer tissues and matched adjacent normal tissues samples. The expression of miR-125a-5p was downregulated in pancreatic cancer cell lines by transfection with miR-125a-5p inhibitor. Cell counting kit-8 assays was conducted to detect the growth ability of pancreatic cancer cell lines. Flow cytometry was applied to detect the cell cycle and apopotosis. Soft agar colony formation test was employed to assess the role of miR-125a-5p in process of malignant transformation.Results MiR-125a-5p was significantly highly expressed in pancreatic ductal adenocarcinoma tissues than adjacent normal tissues(P<0.05). After the expression level of miR-125a-5p in Panc-1 and MIA PaCa-2 was downregulated,the growth ability was suppressed(P<0.05),early apopotosis rate was promoted by 13.6% and 11.0% respectively(P<0.05),the amount of colony formation was reduced by 27.3% and 27.8%,respectively(P<0.05),and the percentage of S stage of Panc-1 was reduced by 11.8% (P<0.05).Conclusions The expression of miR-125a-5p is high in pancreatic ductal adenocarcinoma tissues. After the expression level of miR-125a-5p is downregulated,the growth ability,colony formation,and cell cycle of Panc-1 and MIA PaCa-2 are suppressed,and the early apopotosis rate will be promoted. Therefore,miR-125a-5p may play an oncogenic role in pancreatic ductal adenocarcinoma.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Pancreatic Neoplasms
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Cell Cycle
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Apoptosis
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Carcinoma, Pancreatic Ductal
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MicroRNAs
Limits:
Humans
Language:
En
Journal:
Zhongguo Yi Xue Ke Xue Yuan Xue Bao
Year:
2016
Document type:
Article
Affiliation country:
China
Country of publication:
China