Author/Authors :
Fang، Zhixiong نويسنده Department of Infectious Disease,XiangTan City Central Hospital,XiangTan,China , , He، Langqiu نويسنده Department of Infectious Disease,XiangTan City Central Hospital,XiangTan,China , , Jia، Hui نويسنده Department of Infectious Disease,XiangTan City Central Hospital,XiangTan,China , , Huang، Qiusheng نويسنده Department of Infectious Disease,XiangTan City Central Hospital,XiangTan,China , , Chen، Dan نويسنده Inefections Disease Hospital,Edong Healthcare City Hospital of Traditional Chinese Medicine,Huangshi,China , , Zhang، Zhiwei نويسنده Cancer Research Institute,Key Laboratory of Cancer Cellular and Molecular Pathology,University of South China,Hengyang,China ,
Abstract :
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.
