miR-181d Inhibits Proliferation and Promotes Apoptosis in Colon Cancer Cells
10.3969/j.issn.1671-7414.2017.02.004
- VernacularTitle:miR-181d在结肠癌中表达失调并抑制癌细胞增殖及凋亡
- Author:
Qi WU
;
Gaofei SHEN
;
Lina SUN
;
Xin WANG
;
Lei GENG
;
Feng DU
;
Xiaodi ZHAO
;
Yuanyuan LU
- Keywords:
colon cancer;
miR-181d : proliferation;
apoptosis
- From:
Journal of Modern Laboratory Medicine
2017;32(2):15-18,22
- CountryChina
- Language:Chinese
-
Abstract:
Objective To detect miR-181d expression levels in colon cancer cell lines,and to study the functions of miR-181d on colon cancer cell proliferation and apoptosis.Methods RT qPCR was employed to study miR-181d cxpression levels in colon cancer cell line HCT116,HT29,LoVo,SW480 and SW620 cells,as well as in colon normal epithelial cell line HIEC.miR-181d mimic and control were transfected into LoVo cells while miR-181d inhibitor and control were transfected into SW620 cells.qRT-PCR was performed to validate the transfection efficiency.MTT assay was performed to measure cell proliferation while flow cytometry was performed to detect cell cycle and apoptosis rate.Results miR-181d was universally downregulated in all colon cancer cell lines compared to the colon normal epithelial cell line HIEC (F=29.34,P＜0.01).Overexpression of miR-181d in LoVo cells significantly decreased in vitro cell proliferation rate (F=5.403,P＜0.01).Flow cytometry indicated that cells at S phase were greatly decreased (t=4.71,P＜0.05) and apoptotic cells were gready increased compared to the control cells (t=3.47,P＜0.05).On the contrary,inhibition of miR-181d in SW620 cells significantly promoted cell proliferation (F=20.82,P＜0.01).Cell cycle was accelerated with significant increase in S phase compared to the control cells (t=2.92,P＜0.05),whereas apoptosis rano was significantly decreased (t=4.14,P＜0.05).Conclusion miR-181d was universally downregulated in colon cancer cell lines compared to the normal epithelial cell line.miR-181d inhibits cell proliferation and induces apoptosis,thus functions as an tumor suppressive miRNA.
