The PDGF-D/miR-106a/Twist1 pathway orchestrates epithelial-mesenchymal transition in gemcitabine resistance hepatoma cells

Oncotarget
Rui WangQiong Wu

Abstract

Emerging evidence demonstrates that platelet-derived growth factor-D (PDGF-D) plays a critical role in epithelial-mesenchymal transition (EMT) and drug resistance in hepatocellular carcinoma (HCC) cells. However, the underlying mechanism has not been fully elucidated. The objective is to explore the molecular mechanism of PDGF-D-mediated EMT in drug resistance HCC cells. To achieve our goal, we used multiple approaches including Western blotting, real-time RT-PCR, wound healing assay, invasion assay, luciferase activity assay, transfection, and immunohistochemistry. We found that PDGF-D is highly expressed in gemcitabine-resistant (GR) HCC cells. Moreover, PDGF-D markedly inhibited miR-106a expression and subsequently upregulated Twist1 expression. Notably, PDGF-D expression was associated with miR-106a and Twist1 in HCC patients. Our findings provide a possible molecular mechanism for understanding GR chemoresistance in HCC cells. Therefore, inactivation of PDGF-D/Twist or activation of miR-106a could be a novel strategy for the treatment of HCC.

References

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Citations

Jan 29, 2016·Journal of Experimental & Clinical Cancer Research : CR·Yang LiuQiong Wu
Sep 14, 2018·Frontiers in Oncology·Fabio CorràStefano Volinia
Oct 18, 2019·Cancers·Quirino LaiUNKNOWN Associazione Italiana per lo Studio del Fegato (AISF) HCC Special Interest Group
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Methods Mentioned

BETA
transfection
PCR
protein assay
Assay

Software Mentioned

GraphPad Prism
PicTar
TargetScan
miRanda

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