Isoliquiritigenin inhibits non-small cell lung cancer progression via m6A/IGF2BP3-dependent TWIST1 mRNA stabilization

Yameng Cui1, Yulin Wu2, Cong Wang1

  • 1Department of Integrated Traditional & Western Medicine, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.

Abstract

Insights

Isoliquiritigenin (ISL) inhibits non-small cell lung cancer (NSCLC) by targeting the m6A modification pathway. This study reveals ISL

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) is implicated in non-small cell lung cancer (NSCLC) tumorigenesis.
  • Isoliquiritigenin (ISL), from licorice, exhibits anti-tumor properties.
  • The specific role of ISL in NSCLC via m6A modification remains largely unelucidated.

Purpose of the Study:

  • To investigate the anti-tumor effects of ISL on NSCLC.
  • To determine if ISL modulates m6A modification to affect NSCLC phenotypes.

Main Methods:

  • In vitro assays assessed ISL's impact on NSCLC cell proliferation, migration, and invasion.
  • m6A enrichment was quantified.
  • Mechanism involving IGF2BP3 was explored using RIP-PCR, MeRIP-qPCR, and RNA decay analysis.

Main Results:

  • ISL significantly inhibited NSCLC cell proliferation, migration, and invasion.
  • IGF2BP3 expression was elevated in NSCLC tissues and correlated with poor survival.
  • ISL reduced m6A modification and IGF2BP3 expression, impacting TWIST1 mRNA stability.

Conclusions:

  • ISL demonstrates anticarcinogenic potential in NSCLC.
  • The findings highlight the IGF2BP3/m6A/TWIST1 axis as a therapeutic target for NSCLC.

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