Pentamethylquercetin induces Hep3B liver cancer cell apoptosis and cell cycle arrest via the ERK/NF-?B signaling pathway
In this study, we investigated the biological roles and potential mechanisms of pentamethylquercetin (PMQ), a natural polymethyl flavones, against Hep3B liver cancer cells. Cell viability and growth curves were determined using the cell counting kit-8 (CCK-8) assay; flow cytometry was used to detect cell cycle and apoptosis; colony formation assay and JC-1 staining were used to detect cell proliferation and mitochondrial membrane potential changes, respectively. Transcriptome sequencing and western blotting were respectively used to investigate transcription and expression changes in Hep3B cells treated with PMQ. Treatment with 30 and 100 µM PMQ more significantly inhibited cell growth and proliferation in Hep3B cells than in HepG2 and LO2 cells. PMQ induced Hep3B cell cycle arrest and apoptosis by significantly reducing CDK4, CDK6, Cyclin D1, Cyclin E1, Cyclin B1 and Bcl-2 expression and increasing Bax, CDK1 and cleaved PARP levels. Transcriptomic profiles and western blotting results revealed that the MAPK and TNF signaling pathways may be involved in PMQ-induced Hep3B apoptosis. Overall design: Hep3B cells (three independent replicates per group) were treated with pentamethylquercetin(PMQ) (0, 100 µM) for 24 h.