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Updated: Sep 5, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
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.
Background:
N6-methyladenosine (m6A) has been identified to regulate the tumorigenesis and development of various tumors, including non-small cell lung cancer (NSCLC). Isoliquiritigenin (ISL), derived from the Chinese herb licorice, shows a significant anti-tumor activity on multiple human cancers. However, the role of ISL on NSCLC through m6A is still unclear.
Purpose:
Here, we investigated the anti-tumor effect of ISL on NSCLC, and explored whether ISL affected the NSCLC phenotype by modulating its m6A modification.
Methods:
Cell proliferation, migration and invasion assays were performed to evaluate the inhibitory effects of ISL on NSCLC cells. M6A enrichment was determined by m6A quantitative analysis. The mechanism regarding IGF2BP3 was explored using RIP-PCR, MeRIP-qPCR and RNA decay analysis.
Results:
ISL significantly repressed the proliferation, migration and invasion of NSCLC cells in vitro. In addition, m6A reader IGF2BP3 expression significantly increased in NSCLC tissues compared to adjacent tissues, and was positively correlated with NSCLC patients' poor survival. Mechanistically, ISL reduced m6A modification and down-regulated IGF2BP3 expression in NSCLC. Furthermore, IGF2BP3 enhanced the mRNA stability of twist family bHLH transcription factor 1 (TWIST1) in m6A-dependent manner. Moreover, ISL treatment combined with TWSIT1 knockdown effectively reversed IGF2BP3 overexpression-induced NSCLC cells' proliferation, migration and invasion.
Conclusion:
Our findings uncover that ISL might function as an anticarcinogen through targeting IGF2BP3/m6A/TWIST1 axis for NSCLC.
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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