https://www.selleckchem.com/pr....oducts/Rapamycin.htm
Mechanistically, miR-222-3p was directly bound to the 3'-UTR of THBS1 and acted as its competing endogenous RNA (ceRNA). Interestingly, THBS1 silencing attenuated the inhibitory effect of miR-222-3p downregulation on the proliferation of these cell lines in vitro. Our results revealed that HBV infection further increased miR-222-3p expression and promoted HCC progression via miR-222-3p-mediated THBS1 downregulation. Our findings suggest that miR-222-3p might be a potential diagnostic and therapeutic target for HCC and HBV-related HCC.
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