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METTL3-mediated m6A modification of TP73-AS1 enhances HCC progression by activating Wnt/β-catenin signaling
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DOI：10.1007/s12672-026-05756-w.png)
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Abstract
En 中文
Long noncoding RNAs (lncRNAs) play key roles in the onset and progression of hepatocellular carcinoma (HCC). Tumor protein 73 antisense RNA 1 (TP73-AS1), a recently identified lncRNA, has been implicated in cancer occurrence, drug resistance, and prognosis; however, its function in HCC remains unclear. Here, TP73-AS1 was found to be significantly elevated in HCC. Mechanistically, METTL3-driven m6A modification enhanced TP73-AS1 stability in a YTHDF1-dependent manner. Functionally, TP73-AS1 promoted HCC cell proliferation, migration, and invasion. Furthermore, TP73-AS1 acted as a molecular sponge for hsa-miR-1233-3p, thereby increasing CTNNB1 (β-catenin) expression and activating the Wnt/β-catenin signaling pathway. Taken together, this study identifies TP73-AS1 as a novel oncogenic lncRNA in HCC and reveals a METTL3–m6A–YTHDF1–TP73-AS1/miR-1233-3p/CTNNB1 axis that drives tumor progression, providing potential targets for HCC diagnosis and therapy.
Keywords:
Hepatocellular carcinoma
m6A
β-Catentin/WNT
ceRNA
TP73-AS1
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