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Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
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TRIM59 promotes gefitinib resistance in EGFR mutant lung adenocarcinoma cells

Zhilei Cui1, Zhen Liu2, Junxiang Zeng3

  • 1Department of Respiratory Medicine, XinHua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China.

Life Sciences
|March 24, 2019
PubMed
Abstract

Insights

Overexpression of TRIM59 in lung cancer cells contributes to gefitinib resistance by activating STAT3 signaling. Targeting TRIM59 or STAT3 may overcome drug resistance in EGFR-mutant lung adenocarcinoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The role of TRIM59 in drug resistance remains unclear despite its known functions in human cancers.
  • Gefitinib resistance is a significant challenge in treating EGFR-mutant lung adenocarcinoma.

Purpose of the Study:

  • To investigate TRIM59 expression in gefitinib-resistant EGFR-mutant lung adenocarcinoma cells.
  • To elucidate the mechanism by which TRIM59 contributes to gefitinib resistance.

Main Methods:

  • Established gefitinib-resistant cell lines through progressive dosage.
  • Quantified TRIM59 expression using real-time PCR and Western blot.
  • Assessed cell viability, apoptosis, proliferation, migration, and invasion following TRIM59 knockdown via shRNA.
  • Analyzed TRIM59-STAT3 interaction using co-immunoprecipitation.

Main Results:

  • TRIM59 was overexpressed in gefitinib-resistant cells.
  • TRIM59 knockdown reduced cell viability, induced apoptosis, and suppressed migration/invasion.
  • TRIM59 interacts with STAT3, and its deficiency impairs STAT3 activation.
  • STAT3 knockdown resensitized cells to gefitinib.

Conclusions:

  • Aberrant TRIM59 overexpression is linked to gefitinib resistance in EGFR-mutant lung adenocarcinoma.
  • The TRIM59-STAT3 signaling pathway is implicated in the development of gefitinib resistance.
Keywords:
Gefitinib resistanceNon-small-cell lung cancerPhosphorylationSTAT3TRIM59

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