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NRAV promotes HCC stemness via the m6A-regulated let-7c-5p/LIN28B axis
Yuhang Chen1,2, Suoyi Dai1,2, Liping Zhuang1,2
1Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Cancer Gene Therapy
|December 13, 2025
Summary
Researchers discovered a new molecular pathway involving the NRAV long non-coding RNA (lncRNA) that drives liver cancer (HCC) stemness. This NRAV-let-7c-5p-LIN28B axis, regulated by m6A modification, offers a potential therapeutic target for liver cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Long non-coding RNAs (lncRNAs) are implicated in hepatocellular carcinoma (HCC) pathogenesis.
- The role of N6-methyladenosine (m6A) modification in regulating lncRNAs in HCC is not well understood.
Purpose of the Study:
- To identify and characterize the function of m6A-modified lncRNAs in HCC.
- To elucidate the molecular mechanisms by which these lncRNAs regulate cancer stemness in HCC.
Main Methods:
- Bioinformatics analysis of TCGA data.
- In vitro and in vivo experimental validation in HCC models.
- MeRIP-qPCR and site-directed mutagenesis to confirm m6A modification.
- Correlation analysis with clinical data and cancer stem cell markers.
Main Results:
- NRAV, an m6A-modified lncRNA, is overexpressed in HCC and linked to poor prognosis.
- NRAV promotes HCC stemness by acting as a competing endogenous RNA (ceRNA) for hsa-let-7c-5p, thereby upregulating LIN28B.
- m6A modification of NRAV is essential for its function in promoting stemness.
- NRAV expression correlates with HCC progression and cancer stem cell marker accumulation.
Conclusions:
- A novel molecular axis (NRAV-let-7c-5p-LIN28B) regulated by m6A modification is identified in HCC.
- This axis links m6A modification to the maintenance of cancer stem cells (CSCs) in liver cancer.
- NRAV represents a potential therapeutic target for disrupting CSC pathways in HCC.
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