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DUSP4 promotes doxorubicin resistance in gastric cancer through epithelial-mesenchymal transition

Xing Kang1, Minhuan Li2, Hao Zhu3

  • 1Department of General Surgery, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, Jiangsu Province, China.

Oncotarget
|December 8, 2017
PubMed

Insights

Dual specificity phosphatase 4 (DUSP4) enhances doxorubicin resistance in gastric cancer by promoting the epithelial-mesenchymal transition (EMT). Reducing DUSP4 or blocking EMT increases cancer cell sensitivity to doxorubicin treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Chemoresistance, particularly to doxorubicin, significantly limits treatment effectiveness in gastric cancer.
  • Dual specificity phosphatase 4 (DUSP4) is implicated in tumor progression, but its role in chemoresistance is not fully understood.

Purpose of the Study:

  • To elucidate the mechanism by which DUSP4 influences doxorubicin resistance in gastric cancer cells.
  • To investigate the potential involvement of the epithelial-mesenchymal transition (EMT) in DUSP4-mediated chemoresistance.

Main Methods:

  • Cell viability and proliferation were assessed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays.
  • Protein expression levels of DUSP4, E-cadherin, and Vimentin were analyzed via Western blotting.
  • DUSP4 overexpression and knockdown models were employed, alongside EMT inhibition using Twist siRNA.

Main Results:

  • Overexpression of DUSP4 conferred increased resistance to doxorubicin in gastric cancer cells.
  • Knockdown of DUSP4 significantly enhanced sensitivity to doxorubicin.
  • DUSP4 up-regulation promoted EMT, evidenced by changes in E-cadherin and Vimentin expression; blocking EMT with Twist siRNA increased doxorubicin sensitivity, confirming EMT's role.

Conclusions:

  • DUSP4 enhances doxorubicin resistance in gastric cancer cells.
  • This resistance is mediated through the promotion of the epithelial-mesenchymal transition (EMT).
  • Targeting DUSP4 or the EMT pathway may represent a therapeutic strategy to overcome doxorubicin resistance in gastric cancer.
Keywords:
DUSP4chemoresistancedoxorubicinepithelial-mesenchymal transitiongastric cancer

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