Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/ijms23020913
Keywords
hnRNPQ; EMT; mirRNAs; HCC; RNA binding proteins; metastasis
Funding
- Sapienza University of Rome [RG11916B6A9C42C7, RM11916B6A80C2CF]
- AIRC [IG 26290]
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This study reveals the role of hnRNP-Q in epithelial-mesenchymal transition (EMT) and its regulation of a set of miRNAs, which in turn influences the cellular phenotype and migratory capacity.
Heterogeneous nuclear ribonucleoproteins (hnRNPs) control gene expression by acting at multiple levels and are often deregulated in epithelial tumors; however, their roles in the fine regulation of cellular reprogramming, specifically in epithelial-mesenchymal transition (EMT), remain largely unknown. Here, we focused on the hnRNP-Q (also known as SYNCRIP), showing by molecular analysis that in hepatocytes it acts as a mesenchymal gene, being induced by TGF beta and modulating the EMT. SYNCRIP silencing limits the induction of the mesenchymal program and maintains the epithelial phenotype. Notably, in HCC invasive cells, SYNCRIP knockdown induces a mesenchymal-epithelial transition (MET), negatively regulating their mesenchymal phenotype and significantly impairing their migratory capacity. In exploring possible molecular mechanisms underlying these observations, we identified a set of miRNAs (i.e., miR-181-a1-3p, miR-181-b1-3p, miR-122-5p, miR-200a-5p, and miR-let7g-5p), previously shown to exert pro- or anti-EMT activities, significantly impacted by SYNCRIP interference during EMT/MET dynamics and gathered insights, suggesting the possible involvement of this RNA binding protein in their transcriptional regulation.
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