| Huang Changshan,Yu Wei,Wang Qian,et al.Overexpressing miR-29c targeting AKT2 enhances the radiosensitivity of human hepatocellular carcinoma cell line HepG2[J].Chinese Journal of Radiological Medicine and Protection,2019,39(3):185-191 |
| Overexpressing miR-29c targeting AKT2 enhances the radiosensitivity of human hepatocellular carcinoma cell line HepG2 |
| Received:August 06, 2018 |
| DOI：10.3760/cma.j.issn.0254-5098.2019.03.005 |
| KeyWords:Liver cancer miR-29c AKT2 Radiosensitivity |
| FundProject: |
| Author Name | Affiliation | | Huang Changshan | Hepatobiliary and Pancreatic Surgery, Henan Cancer Hospital, Zhengzhou 450008, China | | Yu Wei | Hepatobiliary and Pancreatic Surgery, Henan Cancer Hospital, Zhengzhou 450008, China | | Wang Qian | Hepatobiliary and Pancreatic Surgery, Henan Cancer Hospital, Zhengzhou 450008, China | | Ye Ke | Department of Radiotherapy, Henan Cancer Hospital, Zhengzhou 450008, China | | Xie Yi | Gastrointestinal Surgery, Henan Provincial People's Hospital, Zhengzhou 450008, China |
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| Abstract:: |
| Objective To investigate the effect of miR-29c on radiosensitivity of hepatoma HepG2 cells by targeting AKT2 gene. Methods The expression of miR-29c in human normal hepatocytes THLE-3 and hepatoma cell HepG2 was detected by RT-PCR. The relationship between miR-29c and AKT2 were predicted by predicted by informative analysis and verified by dual luciferase reporter gene test and Western blot. miR-29c mimic/AKT2 gene recombinant plasmid and miR-29c inhibitor/lentivirus vector AKT2 shRNA were transfected into HepG2 cells by Liposome 2000. The cells were irradiated with different doses (0, 2, 4, 6 and 8 Gy) of X-rays, and the effects of miR-29/AKT2 on the survival and cell viability of HepG2 cells were detected by cloning and MTT assays. Results Compared with THLE-3 cells, the expression of miR-29c in HepG2 cells was significantly lower (t=17.816, P<0.05). After 2, 4, 6 and 8 Gy X-ray irradiation, the survival of HepG2 cells was significantly lower than that of THLE-3 cells (t=4.541, 6.823, 7.218, 9.363, P<0.05), and the expression of miR-29c in HepG2 cells was significantly decreased (t=5.599, 9.262, 10.470, 10.873, P<0.05). The survival and viability of HepG2 cells were decreased by miR-29c overexpression (tsurvival rate=4.307, 7.668, 7.668, 6.894, P<0.05; tcell viability=3.443, 8.116, 13.434, P<0.05) but they were increased by miR-29c inhibition (tsurvival rate=4.003, 6.713, 7.141, P<0.05; tcell viability=4.282, 5.113, P<0.05). Double luciferase reporter gene experiments showed that AKT2 was the target gene of miR-29c since the expression of AKT2 was negatively regulated by miR-29c. After the silence of AKT2 or overexpression of AKT2, the survival and viability of HepG2 cells were consistent with the overexpression of miR-29c or the inhibition of miR-29c, respectively. Conclusions MiR-29c increases the radiosensitivity of hepatoma cell HepG2 by targeting AKT2. |
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