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GLP2-GLP2R signal affects the viability and EGFR-TKIs sensitivity of PC9 and HCC827 cells

Bin Song1, Hong Ge1, Chenwei Pu1

  • 1Department of Respiratory Medicine, Zibo Central Hospital, #54 Gongqingtuan West Road, Zhangdian, Zibo, 255036, Shandong, People's Republic of China.

BMC Pulmonary Medicine
|January 14, 2022
PubMed
Abstract

Insights

Glucagon-like peptide 2 (GLP-2) receptor signaling enhances lung cancer cell resistance to EGFR-TKIs and cisplatin. Inhibiting GLP-2 or GLP2R may improve cancer treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Lung cancer treatment faces challenges due to resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs).
  • Understanding novel signaling pathways involved in drug resistance is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of glucagon-like peptide (GLP)-2 and GLP-2 receptor (GLP2R) signaling in acquired resistance to EGFR-TKIs and cisplatin in lung cancer cells.
  • To identify potential therapeutic targets for overcoming drug resistance.

Main Methods:

  • Screening of differentially expressed genes in EGFR-TKI-resistant lung cancer cell lines (PC9, HCC827) using public datasets (GSE168043, GSE163913).
  • Western blot analysis to detect GLP2R expression in resistant cells.
  • CCK-8 and flow cytometry assays to assess the impact of GLP2R modulation (up-regulation/down-regulation) on drug sensitivity.
  • Treatment of parental cells with teduglutide, a GLP-2 analog.

Main Results:

  • 143 common differentially expressed genes were identified between parent and resistant cells.
  • GLP2R expression was significantly upregulated in drug-resistant lung cancer cell lines.
  • Overexpression of GLP2R enhanced cell viability, while GLP2R knockdown reduced viability in resistant cells.
  • Teduglutide treatment increased lung cancer cell viability.

Conclusions:

  • The GLP-2/GLP2R signaling pathway appears to modulate lung cancer cell sensitivity to EGFR-TKIs and cisplatin.
  • Targeting GLP-2 or GLP2R with inhibitors could represent a promising strategy for improving clinical outcomes in lung cancer treatment.
Keywords:
CisplatinEGFR-TKIs therapyGLP2RLung cancer

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