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Updated: Jun 9, 2025

Radiosensitivity of Cancer Stem Cells in Lung Cancer Cell Lines
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The NEDD4/FLRT2 axis regulates NSCLC cell stemness.

Yuping Yang1,2, Fei Yan3, Ziwei Gao1,2

  • 1Department of Respiratory and Critical Care Medicine, School of Clinical Medicine and The First Affiliated Hospital of Chengdu Medical College, School of Clinical Medicine, of Chengdu Medical College, Chengdu, China.

Frontiers in Pharmacology
|October 24, 2024
PubMed
Summary
This summary is machine-generated.

Fibronectin leucine-rich transmembrane 2 (FLRT2) inhibits non-small cell lung cancer (NSCLC) stemness and tumorigenesis. E3 ligase NEDD4 degrades FLRT2, promoting NSCLC progression and counteracting FLRT2

Keywords:
FLRT2Nedd4degradationnon-small cell lung cancerstemness

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Lung cancer is a leading cause of cancer-related death, with non-small cell lung cancer (NSCLC) posing significant treatment challenges.
  • Cancer stem cells (CSCs) play a crucial role in the development and progression of NSCLC.
  • The neuronally expressed developmentally downregulated 4 (NEDD4) and fibronectin leucine-rich transmembrane 2 (FLRT2) axis warrants investigation for its role in NSCLC stemness.

Purpose of the Study:

  • To investigate the influence of the NEDD4-FLRT2 axis on cancer stemness in NSCLC.
  • To elucidate the underlying molecular mechanisms by which NEDD4 and FLRT2 regulate NSCLC stem cell properties.

Main Methods:

  • Western blot and RT-qPCR to assess FLRT2 expression in NSCLC tissues and stem cells.
  • Sphere formation assays and stemness marker analysis to confirm NSCLC stemness.
  • Cell proliferation, migration, apoptosis assays, and xenograft mouse models to evaluate antitumor effects and tumorigenesis in vivo.
  • Co-immunoprecipitation (Co-IP) assays to confirm the interaction between NEDD4 and FLRT2.

Main Results:

  • FLRT2 expression was found to be reduced in NSCLC tissues, cells, and NSCLC stem cells.
  • FLRT2 upregulation inhibited NSCLC stem cell proliferation, sphere formation, and drug resistance, while promoting apoptosis.
  • NEDD4 was identified as an E3 ligase that promotes the ubiquitination and degradation of FLRT2 protein.
  • NEDD4 overexpression counteracted the inhibitory effects of FLRT2 on NSCLC stemness, both in vitro and in vivo.

Conclusions:

  • FLRT2 functions as a tumor suppressor in NSCLC by inhibiting cancer stemness.
  • NEDD4 promotes NSCLC stem cell tumorigenesis by enhancing the degradation of FLRT2.
  • Targeting the NEDD4-FLRT2 axis may offer a novel therapeutic strategy for NSCLC treatment.