ArticlePloS one2025
MiR-122 promotes metastasis of hepatoma cells by modulating RBM47-integrin alpha V-TGF-beta signaling.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Epithelial Integrins Coordinate Cellular Crosstalk Through the Regulation of Cytokines During Tissue Remodeling.International journal of molecular sciences · 2026Review
- RNA-binding motif proteins as context-dependent regulators of tumor-immune crosstalk, genome stability, and therapeutic vulnerabilities in cancer.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MiR-122 is a liver-abundant miRNA, which is thought to harbor antitumorigenic activity. Elevated transforming growth factor-β (TGF-β) in hepatocellular carcinoma (HCC) microenvironment is a potent inducer for tumor metastasis. However, the involvement of miR-122 in regulation of TGF-β signaling and its implication in TGF-β-related HCC metastasis remains obscure. In this study, we demonstrated that miR-122 significantly enhanced the activities of the TGF-β pathway reporter, the levels of phosphorylation of Smad2 and Smad3, and the expression of mesenchymal markers (N-cadherin and vimentin) in HCC cells. Notably, miR-122 significantly promoted the migration and invasion in vitro and pulmonary metastasis of HCC cells in vivo. Mechanism investigations revealed that miR-122 directly suppressed the expression of RBM47, which was a novel RNA binding protein. RBM47 decreased the level of αv integrin (ITGAV) by promoting the degradation of mRNA via interacting with the AU-rich elements in its 3'UTR. Subsequently, the elevated ITGAV induced by miR-122 promoted activation of the latent TGF-β, thereby boosted the TGF-β signaling and then promoted cell motility. Taken together, miR-122 could promote metastasis of hepatoma cells by regulating RBM47-ITGAV-TGF-β signaling. These findings provide new insight into the regulatory network of miR-122, the complexity and robustness of TGF-β pathway and the mechanisms of HCC metastasis.
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