Effect of mitofusion 2 on the proliferation of prostate cancer cells
10.3760/cma.j.issn.1006-9801.2018.04.012
- VernacularTitle:线粒体融合蛋白2对前列腺癌细胞增殖的影响
- Author:
Geng HUANG
1
;
Weidong JIANG
;
Qing MAO
;
Dingwen GUI
Author Information
1. 435000,湖北理工学院附属医院 鄂东医疗集团黄石市中心医院泌尿外科 肾脏疾病发生与干预湖北省重点实验室
- Keywords:
Prostate neoplasms;
Mitofusion 2;
Cell cycle;
Proliferation
- From:
Cancer Research and Clinic
2018;30(4):266-269
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of mitofusion 2 (MFN2) on the proliferation of prostate cancer cells and its molecular mechanism. Methods Lentivirus containing the MFN2 coding sequence (Lenti-MFN2) were used to infect the prostate cancer cell lines DU-145 and LNCaP, and the lentivirus containing the green fluorescent protein gene (Lenti-GFP) were defined as the control. Real-time quantitative PCR (qRT-PCR) and Western blot were used to detect the expression of MFN2 mRNA and protein in the infected cells. MTT assay and colony formation assay were used to detect the cell proliferation. Cell cycle distribution was measured by flow cytometry.Western blot was used to detect the expression of Ras,p-Raf and p-Erk1/2 proteins in infected cells. Results The expressions of MFN2 mRNA in DU-145 and LNCaP cells of Lenti-MFN2 group were 2.79±0.91 and 3.87±1.06, which were higher than those in Lenti-GFP group (1.02± 0.27 and 1.13±0.59),the differences were statistically significant(t=3.726,P=0.010;t=5.209,P =0.002). Compared with Lenti-GFP group, the expression of MFN2 protein in Lenti-MFN2 group was increased. The number of colonies formed in DU-145 and LNCaP cells of Lenti-MFN2 group was 147.42±32.91 and 130.26± 62.47, respectively, which was lower than that of the Lenti-GFP group (255.46±50.91 and 238.10±49.77), the differences were statistically significant (t =3.565, P=0.012; t =2.700, P=0.036). The cell cycle was arrested at G0/G1phase,and the expressions of Ras, p-Raf and p-Erk1/2 proteins were significantly decreased. Conclusion MFN2 can inhibit the proliferation of prostate cancer cells,and its mechanism may be related to the inhibition of activation of Ras-Raf1-Erk1/2 signaling pathway.
