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LTBP2 regulates cisplatin resistance in GC cells via activation of the NF-κB2/BCL3 pathway

Jun Wang1, Wenjia Liang2, Xiangwen Wang1

  • 1The First Hospital of Lanzhou University, Department of General Surgery, Ward 6, Lanzhou, Gansu, China.

Genetics and Molecular Biology
|April 5, 2024
PubMed

Insights

Silencing latent transforming growth factor β-binding protein 2 (LTBP2) enhances cisplatin sensitivity in gastric cancer by inhibiting the NF-κB2 pathway. This suggests LTBP2 is a potential therapeutic target for overcoming drug resistance.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Gastric cancer (GC) frequently develops resistance to cisplatin chemotherapy.
  • Latent transforming growth factor β-binding protein 2 (LTBP2) is implicated in GC, but its role in cisplatin resistance remains unclear.

Purpose of the Study:

  • To investigate the role of LTBP2 in cisplatin resistance in gastric cancer.
  • To elucidate the molecular mechanisms underlying LTBP2's influence on chemoresistance.

Main Methods:

  • Assessed LTBP2 expression in GC cell lines.
  • Performed cell viability assays to correlate LTBP2 expression with cisplatin sensitivity.
  • Utilized lentivirus-mediated LTBP2 silencing and gene overexpression in GC cells.
  • Analyzed the NF-κB2/Bcl-3/cyclin D1 signaling pathway.

Main Results:

  • LTBP2 silencing in HGC-27 cells enhanced cisplatin sensitivity, reduced proliferation, and inhibited the NF-κB2/Bcl-3/cyclin D1 pathway.
  • Overexpression of NFκB2 in LTBP2-silenced cells restored cisplatin sensitivity and upregulated p52/Bcl-3/cyclin D1.
  • LTBP2 silencing effectively inhibited cell proliferation and mitigated cisplatin resistance.

Conclusions:

  • LTBP2 silencing overcomes cisplatin resistance in gastric cancer by targeting the noncanonical NF-κB2 p52/Bcl-3/cyclin D1 pathway.
  • LTBP2 represents a promising therapeutic target for enhancing cisplatin efficacy in gastric cancer patients.

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