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Mcl-1 stabilization confers resistance to taxol in human gastric cancer

Wu Shuang1, Lili Hou2, Yan Zhu3

  • 1Department of Immunology, Anhui Medical University, Hefei, China.

Oncotarget
|November 16, 2017
PubMed

Insights

Upregulation of Myeloid cell leukemia-1 (Mcl-1) causes acquired Taxol resistance in gastric cancer by stabilizing Mcl-1 via the PI3K/Akt pathway. Inhibiting Mcl-1 or PI3K/Akt reverses this resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Taxol is a key antineoplastic drug for gastric cancer.
  • Acquired Taxol resistance limits its therapeutic effectiveness.
  • Understanding resistance mechanisms is crucial for developing new treatments.

Purpose of the Study:

  • To identify mechanisms of acquired Taxol resistance in human gastric cancer.
  • To investigate the role of Myeloid cell leukemia-1 (Mcl-1) in Taxol resistance.
  • To explore the involvement of the PI3K/Akt signaling pathway.

Main Methods:

  • Investigated Mcl-1 expression and stability in Taxol-resistant gastric cancer cells.
  • Analyzed the activation status of the PI3K/Akt signaling pathway.
  • Assessed the effects of Mcl-1 and PI3K/Akt inhibition on Taxol resistance.

Main Results:

  • Upregulation and stabilization of Mcl-1 were observed in Taxol-resistant cells.
  • Hyper-activation of the PI3K/Akt pathway was linked to Mcl-1 stabilization.
  • Increased Mcl-1 inhibited Taxol-induced apoptosis by preventing mitochondrial outer membrane permeabilization.
  • Inhibition of Mcl-1 or PI3K/Akt reversed the Taxol-resistant phenotype.

Conclusions:

  • Mcl-1 upregulation, driven by PI3K/Akt hyper-activation, confers acquired Taxol resistance in gastric cancer.
  • Mcl-1 acts by blocking Taxol-induced apoptosis.
  • The PI3K/Akt pathway is a critical regulator of Taxol acquired resistance.
  • Mcl-1 represents a potential therapeutic target for overcoming Taxol resistance in gastric cancer.
Keywords:
Mcl-1PI3K/AktTaxol-resistance

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