Collectively, this study presented evidence that miR-206 was controlled by lncRNA MALAT1 and partially suppressed the proliferation and invasion of HCC through the c-Met/Akt/mTOR signaling pathway. According to these results, understanding MALAT1/miR-206-dependent regulation may lead to potential approaches for diagnosis and prospective treatment of HCC.
3PO did not prevent miR-26b-induced SKOV3 migration. Overall, these results support the inverse relation between endogenous miRNA levels and their tumor-suppressive effects and suggest that restoring miR-206 expression represents a potential dual anti-PFKFB3/FAK strategy to control ovarian cancer progression.
Moreover, SOX9 was a target of miR-206, and miR-206 negatively regulated SOX9 expression. Collectively, miR-206 might be a promising biomarker with diagnostic and prognostic value for LC, and the miR-206/SOX9 axis might be a candidate target for LC therapy.