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SYNCRIP Modulates the Epithelial-Mesenchymal Transition in Hepatocytes and HCC Cells.

International journal of molecular sciences (2022-01-22)
Veronica Riccioni, Flavia Trionfetti, Claudia Montaldo, Sabrina Garbo, Francesco Marocco, Cecilia Battistelli, Alessandra Marchetti, Raffaele Strippoli, Laura Amicone, Carla Cicchini, Marco Tripodi
ABSTRACT

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 TGFβ 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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Sigma-Aldrich
Monoclonal Anti-Fibronectin antibody produced in mouse, clone IST-4, ascites fluid
Sigma-Aldrich
Anticorpo anti-hnRNP Q, clone 7A11.2, clone 7A11.2, from mouse