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Induction and Analysis of Epithelial to Mesenchymal Transition
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PDCD2 sensitizes HepG2 cells to sorafenib by suppressing epithelial‑mesenchymal transition

Hongyu Liu1, Min Wang2, Na Liang3

  • 1Department of Hepatobiliary‑Pancreatic Surgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.

Molecular Medicine Reports
|January 22, 2019
PubMed

Insights

Programmed cell death domain 2 (PDCD2) sensitizes liver cancer cells to sorafenib by reducing the epithelial-mesenchymal transition (EMT) and overcoming multidrug resistance (MDR). This finding offers a potential therapeutic target for sorafenib-resistant liver cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Epithelial-mesenchymal transition (EMT) is linked to therapeutic resistance in cancer.
  • Programmed cell death domain 2 (PDCD2) plays a role in cancer progression, but its function in liver cancer chemoresistance is unclear.

Purpose of the Study:

  • To investigate the role of PDCD2 in sorafenib resistance in liver cancer.
  • To elucidate the mechanism by which PDCD2 affects chemoresistance and EMT in liver cancer cells.

Main Methods:

  • Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were used to assess gene and protein expression.
  • Cell Counting Kit-8, Annexin V/fluorescein isothiocyanate, and cell migration assays were employed to evaluate cell viability, apoptosis, and metastasis.

Main Results:

  • Sorafenib-resistant HepG2 cells displayed EMT, multidrug resistance (MDR), and reduced PDCD2 expression.
  • PDCD2 overexpression promoted sorafenib-induced apoptosis and reduced metastasis in liver cancer cells.
  • PDCD2 inhibited Vimentin and increased E-cadherin expression in a Snail-dependent manner, thereby downregulating EMT.

Conclusions:

  • PDCD2 sensitizes sorafenib-resistant liver cancer cells to sorafenib by downregulating EMT.
  • PDCD2 represents a potential therapeutic target for overcoming sorafenib resistance in liver cancer.

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