Dihydroartemisinin inhibits the viability of cervical cancer cells by upregulating caveolin 1 and mitochondrial carrier homolog 2: Involvement of p53 activation and NAD(P)H:quinone oxidoreductase 1 downregulation.

摘要: Dihydroartemisinin (DHA) has been shown to inhibit the viability of various cancer cells. Previous studies have revealed that mechanisms involved in inhibitory effects DHA are based on theactivation p53 and mitochondrial-related cell death pathway. However, exact association between upstream signaling activation pathway remains unclear. In this study, we found treatment induced upregulation caveolin 1 (Cav1) mitochondrial carrier homolog 2 (MTCH2) HeLa cells, was associated with DHA-induced inhibition apoptosis. Additionally, overexpression Cav1 MTCH2 cells enhanced viability. Moreover, also contributed DHA-mediated downregulation redox enzyme, NAD(P)H:quinone oxidoreductase (NQO1), which reported contribute Of note, nuclear translocation accumulation both p53, indicating a novel potential mechanism, namely regulation by Cav1. On whole, our study identified as molecular targets new link Cav1/MTCH2 downstream