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CELF2 Is a Tumor Suppressor That Modulates SLC7A11 and Promotes Ferroptosis in Stomach Adenocarcinoma

Shoucai Zhang1,2, Shichao Liu1,2, Zeyu Zhang1,2

  • 1Department of Clinical Laboratory, Qilu Hospital of Shandong University, Jinan, P.R. China.

Molecular Cancer Research : MCR
|June 17, 2026
PubMed

Insights

CUGBP Elav-like family member 1 (CELF2) acts as a tumor suppressor in stomach adenocarcinoma (STAD) by promoting ferroptosis. CELF2 targets SLC7A11, enhancing ferroptosis susceptibility and inhibiting STAD growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Death Research

Background:

  • Stomach adenocarcinoma (STAD) is a major global gastrointestinal malignancy.
  • Ferroptosis, a distinct form of programmed cell death, is increasingly recognized for its role in cancer.
  • Understanding ferroptosis regulators in STAD is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the role of CUGBP Elav-like family member 1 (CELF2) in stomach adenocarcinoma (STAD).
  • To elucidate the mechanism by which CELF2 influences ferroptosis in STAD.
  • To explore the potential of CELF2 as a therapeutic target for STAD.

Main Methods:

  • Analysis of CELF2 expression in STAD tissues (mRNA and protein).
  • In vitro and in vivo experiments assessing CELF2's effect on STAD cell growth and migration.
  • RNA sequencing (RNA-seq) to identify CELF2-regulated pathways, including glutathione metabolism and ferroptosis.
  • Biochemical assays to measure ferroptosis markers (ROS, MDA, Fe²⁺, 4-HNE, GSH).
  • RNA immunoprecipitation (RIP) and RNA pull-down assays to confirm CELF2-SLC7A11 interaction.

Main Results:

  • CELF2 expression was significantly downregulated in STAD tissues.
  • CELF2 overexpression inhibited STAD cell proliferation and migration in vitro and in vivo.
  • CELF2 promoted ferroptosis by increasing ROS, MDA, Fe²⁺, and 4-HNE levels while decreasing GSH.
  • CELF2 directly interacted with Solute carrier family 7 member 11 (SLC7A11), a key regulator of ferroptosis.
  • SLC7A11 overexpression counteracted the anti-tumor and ferroptosis-inducing effects of CELF2.
  • Ferrostatin-1 treatment rescued CELF2-induced inhibition of STAD cell proliferation.

Conclusions:

  • CELF2 functions as a tumor suppressor in STAD.
  • CELF2 promotes ferroptosis in STAD cells by targeting SLC7A11.
  • CELF2 enhances STAD cell susceptibility to ferroptosis.
  • Targeting CELF2 and the ferroptosis pathway presents a promising therapeutic avenue for STAD.

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