Abstract
ObjectiveThe aim of this study was to investigate the role of XPD in migration and invasion of hepatocellular carcinoma (HCC) cells.MethodsThe expression of XPD and miR-29a-3p was examined by western blot and qRT-PCR, cell proliferation was detected by MTT assay, cell migration was detected by transwell assay. TargetScan was used to predict potential targets of miR-29a-3p.ResultsIn this study, we found that the expression of XPD and miR-29a-3p was downregulated in HCC samples and HCC cell lines. XPD suppressed proliferation and migration of HCC cell via regulating miR-29a-3p expression. Target prediction analysis and dual-luciferase reporter assay confirmed Mdm2 and PDGF-B were direct targets of miR-29a-3p, and miR-29a-3p suppressed proliferation and migration of HCC cells via regulating the expression of Mdm2 or PDGF-B.ConclusionsOur data indicated that XPD suppressed cell proliferation and migration via miR-29a-3p-Mdm2/PDGF-B axis in HCC.
Highlights
Hepatocellular carcinoma (HCC) is a primary neoplasm of the liver and the sixth most common solid tumor and the third most lethal malignancy globally [1]
Emerging evidence indicates that Xeroderma pigmentosum D (XPD) could prime cell cycle arrest, induce HCC apoptosis and inhibit its viability [9], which implicated that XPD may reverse the malignant phenotype of hepatoma cells by repairing the damaged DNA
MiR-29a-3p RNA level was lower in tumor tissues than non-tumor tissues (Fig. 1c), and miR-29a-3p expression was positively associated with XPD expression in HCC samples (Fig. 1d)
Summary
Hepatocellular carcinoma (HCC) is a primary neoplasm of the liver and the sixth most common solid tumor and the third most lethal malignancy globally [1]. Since effectively diagnosing HCC at its early stage is difficult, only 20% of HCC patients are amenable to curative therapy by liver transplant, surgical resection, or ablative therapy, and even some of these patients suffer from the recurring tumors [2, 3]. The liver is pivotal for many metabolic functions [7] and is very susceptible to carcinogenesis as the oxidant byproducts of hepatocellular metabolism often induced DNA damage. Emerging evidence indicates that XPD could prime cell cycle arrest, induce HCC apoptosis and inhibit its viability [9], which implicated that XPD may reverse the malignant phenotype of hepatoma cells by repairing the damaged DNA. We further investigated the influence of XPD on hepatoma cell proliferation in the molecular mechanism perspective
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