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• W1915692470 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." @default.
• W1915692470 created "2016-06-24" @default.
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• W1915692470 date "2015-02-11" @default.
• W1915692470 modified "2023-10-16" @default.
• W1915692470 title "The PDGF-D/miR-106a/Twist1 pathway orchestrates epithelial-mesenchymal transition in gemcitabine resistance hepatoma cells" @default.
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• W1915692470 doi "https://doi.org/10.18632/oncotarget.3193" @default.
• W1915692470 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4466665" @default.
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• W1915692470 hasPublicationYear "2015" @default.
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