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  11. Igf2bp3 Suppresses Ferroptosis In Lung Adenocarcinoma By M6a-dependent Regulation Of Tfap2a To Transcriptionally Activate Slc7a11/gpx4

IGF2BP3 suppresses ferroptosis in lung adenocarcinoma by m6A-dependent regulation of TFAP2A to transcriptionally activate SLC7A11/GPX4

Pengpeng Li1, Dan Chu2, Guangcheng Ding1

  • 1Tumor Treatment Center, The Fifth Affiliated Hospital of Zhengzhou University, No. 3 Kangfuqian Street, Erqi District, Zhengzhou, 450052, China.

Molecular and Cellular Biochemistry
|July 18, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) suppresses ferroptosis in lung adenocarcinoma by stabilizing transcription factor AP-2 alpha (TFAP2A) via m6A modification, promoting SLC7A11 and GPX4 transcription. Targeting this axis may enhance ferroptosis sensitivity in LUAD.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Ferroptosis, a form of regulated cell death, is implicated in tumor development.
  • Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) is an oncogene in lung adenocarcinoma (LUAD).
  • The role of IGF2BP3 in regulating ferroptosis in LUAD remains largely unexplored.

Purpose of the Study:

  • To investigate the mechanism by which IGF2BP3 regulates ferroptosis in LUAD.
  • To elucidate the relationship between IGF2BP3, transcription factor AP-2 alpha (TFAP2A), and ferroptosis-related genes.
  • To explore the therapeutic potential of targeting the IGF2BP3/TFAP2A pathway in LUAD.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) and Western blot to assess gene and protein expression.
  • Cell viability assays (CCK-8), reactive oxygen species (ROS) detection (DCFH-DA, C11-BODIPY), and oxidative stress marker analysis (MDA, GSH).
Keywords:
FerroptosisGPX4IGF2BP3Lung adenocarcinoma

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  • RNA immunoprecipitation (m6A-RIP, RIP), RNA stability assays, chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays to confirm molecular interactions and transcriptional regulation. In vivo studies using a mice xenotransplant model.

    • Main Results:

    • IGF2BP3 and TFAP2A were highly expressed in LUAD tissues.
    • Knockdown of IGF2BP3 or TFAP2A induced ferroptosis, characterized by increased ROS and MDA, and decreased GSH synthesis and cystine uptake.
    • IGF2BP3 stabilized TFAP2A expression through m6A modification, and TFAP2A promoted the transcription of SLC7A11 and GPX4.
    • IGF2BP3 depletion suppressed LUAD tumor growth in vivo by inducing ferroptosis.

    Conclusions:

    • IGF2BP3 suppresses ferroptosis in LUAD by stabilizing TFAP2A via m6A modification, subsequently promoting the transcription of SLC7A11 and GPX4.
    • The IGF2BP3/TFAP2A/SLC7A11/GPX4 axis represents a novel regulatory pathway in LUAD ferroptosis.
    • Targeting this axis offers a potential therapeutic strategy to enhance ferroptosis sensitivity in LUAD.
    N6-methyladenosine
    SLC7A11
    TFAP2A