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CELF2 suppresses non-small cell lung carcinoma growth by inhibiting the PREX2-PTEN interaction

Yiu To Yeung1,2, Suyu Fan1, Bingbing Lu1,3

  • 1The China-US (Henan) Hormel Cancer Institute, Zhengzhou, Henan, China.

Carcinogenesis
|June 27, 2019
PubMed

Insights

CELF2 enhances tumor suppression by interacting with PREX2, thereby increasing PTEN activity. This mechanism inhibits cancer cell proliferation and improves patient prognosis, particularly in lung adenocarcinoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The phosphoinositide 3-kinase (PI3-K)/Akt pathway regulates cell proliferation and is often dysregulated in cancers.
  • PTEN protein negatively regulates the PI3-K/Akt pathway by dephosphorylating PIP3.
  • PREX2 inhibits PTEN activity, while CELF2 is known to act as a tumor suppressor, but its mechanism with PTEN is unclear.

Purpose of the Study:

  • To elucidate the mechanism by which CELF2 enhances PTEN tumor suppressor activity.
  • To investigate the role of CELF2 in regulating the PI3-K/Akt pathway and cancer cell proliferation.
  • To assess the clinical relevance of CELF2 in lung adenocarcinoma and other cancers.

Main Methods:

  • Investigated the interaction between CELF2 and PREX2 using biochemical assays.
  • Assessed PTEN phosphatase activity upon CELF2 overexpression.
  • Evaluated the effect of CELF2 on Akt phosphorylation and cell proliferation in vitro.
  • Performed ex vivo studies using patient-derived xenografts (PDX) with CELF2 gene delivery.
  • Analyzed CELF2 protein expression and its correlation with prognosis in clinical lung adenocarcinoma samples.
  • Examined CELF2 gene location and expression patterns in The Cancer Genome Atlas (TCGA) datasets for various cancers.

Main Results:

  • CELF2 directly interacts with PREX2, reducing PREX2's association with PTEN.
  • CELF2 overexpression leads to upregulated PTEN phosphatase activity.
  • Overexpression of CELF2 inhibits Akt phosphorylation and cell proliferation, dependent on PTEN presence.
  • CELF2 gene delivery significantly inhibited PDX tumor growth.
  • CELF2 protein expression is downregulated in lung adenocarcinoma tissues and correlates with poor prognosis.
  • CELF2 expression is associated with shorter survival times in multiple cancers, including breast invasive carcinoma, low-grade glioma, and glioblastoma.

Conclusions:

  • CELF2 antagonizes the oncogenic effect of PREX2 by disrupting the PREX2-PTEN interaction, thereby enhancing PTEN tumor suppressor function.
  • CELF2 acts as a novel regulator of the PI3-K/Akt signaling pathway.
  • CELF2 downregulation in tumors suggests its potential as a prognostic biomarker and therapeutic target in various cancers.

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