RESUMO
OBJECTIVE: Our previous study found KCTD10 negatively regulates Notch signaling, but whether KCTD10 regulates human hepatocellular carcinoma (HCC) carcinogenicity was uncertain. METHODS: We used lentivirus infection to regulate KCTD10 expression in HCC cell lines, then monitored tumor sphere formation rate, cell migration, in vitro and in vivo tumorigenicity, cancer stem cell (CSC) biomarkers and Notch signaling variation. RESULTS: Down-regulation of KCTD10 in HCC cell lines (Hep3B and MHCC97H) enhanced the expression of CSC marker genes, promoted self-renewal and tumorigenic ability, and increased the CD133+ cell population. Further molecular studies showed that the transmembrane/intracellular region (NTM) of Notch1 decreased when KCTD10 was knocked down in HCC cell lines, and that the balance between P53 and Notch activity was regulated. CONCLUSIONS: The results demonstrated that KCTD10 can act as a tumor suppressor in HCC cells through Notch signaling.
