The miR-383-LDHA axis regulates cell proliferation, invasion and glycolysis in hepatocellular cancer
نویسندگان
1 Department of Infectious Disease, XiangTan City Central Hospital, XiangTan, People's Republic of China
2 Edong Healthcare City Hospital of Traditional Chinese Medicine, Inefections Disease Hospital, Huangshi, People's Republic of China
3 Cancer Research Institute, University of South China, Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan Provincial University, Hengyang, People's Republic of China
4 Department of Infectious Disease, XiangTan City Central Hospital, XiangTan, People's Republic of China
5 Department of Infectious Disease, XiangTan City Central Hospital, XiangTan, People's Republic of China
6 Department of Infectious Disease, XiangTan City Central Hospital, XiangTan, People's Republic of China
doi
10.22038/ijbms.2017.8246چکیده
Objective(s): To explore the correlation between expression patterns and functions of miR-383 and LDHA in hepatocellular cancer (HCC). Materials and Methods: We detected the expression of miR-383 and LDHA in 30 HCC tissues and their matched adjacent normal tissues using qRT-PCR. Then we performed MTT assay, foci formation assay, transwell migration assay, glucose uptake assay and lactate production assay to explore the function of miR-383 in cell proliferation, invasion and glycolysis in HCC cell lines. Luciferase reporter assay was used to explore whether LDHA was a target gene of miR-383. Western blot and qRT-PCR were used to further confirm LDHA was targeted by miR-383. Then the above functional experiments were repeated to see whether the function of LDHA could be inhibited by miR-383. Results: The results of qRT-PCR showed that miR-383 was down-regulated in HCC tissues compared with their matched adjacent normal tissues. Functional experiments showed that overexpression of miR-383 significantly suppressed cell proliferation, invasion and glycolysis. Luciferase reporter assay showed LDHA was a target gene of miR-383 and expression of LDHA was inversely correlated with that of miR-383 in HCC. Besides, increased cell proliferation, invasion and glycolysis triggered by LDHA could be inhibited by overexpression of miR-383 in HCC cell lines. Conclusion: Our study proved that miR-383 is down-regulated in HCC and acts as a tumor suppressor through targeting LDHA. Targeting the miR-383-LDHA axis might be a promising strategy in HCC treatment.