Journal of clinical laboratory analysis · 2020
Downregulation of miR-1225-5p is pivotal for proliferation, invasion, and migration of HCC cells through NFκB regulation.
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Liu Lin, Zhang Weiguo, Hu Yujing, Ma Liangliang, Xu Xiangsu
Аннотация
BACKGROUND: As one of the most frequently seen malignancies, hepatocellular carcinoma (HCC) serves as the second largest contributor to malignancy-specific mortality worldwide. MicroRNA-1225-5p (miR-1225) exerts an essential impact on the growth and metastasis of many malignancies. However, the contribution of miR-125 to HCC and the molecular mechanism of cancer cell viability and apoptosis are still unclear. We focused our research on exploring the function and molecular mechanism of miR-1225 in regulating HCC cell growth, migration, and invasion.
MATERIAL: Quantitative PCR data showed that miR-1225 expression was repressed in HCC cell lines and in the tissues of HCC patients, compared to that in normal human hepatic cells and tissues. Transfection of a miR-1225 mimic inhibited cell viability and proliferation as indicated by CCK-8 staining and MTT assay. Transwell invasion, wound healing assay, and Western blotting were performed to assess whether miR-1225 repressed the metastasis and invasion of HCC cells, and decreased matrix metalloproteinase 9 (MMP9) expression. Further bioinformatic prediction and dual-luciferase reporter assay suggested that miR-1225 targeted the 3'-UTR of NFκB p65.
RESULTS: Overexpression of p65 protein counteracted the repressive impact of miR-1225 on invasion, migration, and proliferation of HCC cells.
CONCLUSION: This research provided new evidences that miR-1225 inhibits the viability, migration, and invasion of HCC cells by downregulation of p65.
MATERIAL: Quantitative PCR data showed that miR-1225 expression was repressed in HCC cell lines and in the tissues of HCC patients, compared to that in normal human hepatic cells and tissues. Transfection of a miR-1225 mimic inhibited cell viability and proliferation as indicated by CCK-8 staining and MTT assay. Transwell invasion, wound healing assay, and Western blotting were performed to assess whether miR-1225 repressed the metastasis and invasion of HCC cells, and decreased matrix metalloproteinase 9 (MMP9) expression. Further bioinformatic prediction and dual-luciferase reporter assay suggested that miR-1225 targeted the 3'-UTR of NFκB p65.
RESULTS: Overexpression of p65 protein counteracted the repressive impact of miR-1225 on invasion, migration, and proliferation of HCC cells.
CONCLUSION: This research provided new evidences that miR-1225 inhibits the viability, migration, and invasion of HCC cells by downregulation of p65.