Peiminine is a compound that is isolated from Bolbostemma paniculatum (Maxim) Franquet (Cucurbitaceae family), which has demonstrated antitumor activities. Its precise molecular mechanisms underlying antitumor activity remain elusive. In this study, peiminine-induced apoptosis towards human hepatocellular carcinoma and its molecular mechanisms were investigated. MTT assay was employed to assess anticancer effects of peiminine at concentrations of 2, 4, 6, 8, 10, 12, and 14 μg/ml after 24, 48, or 72 h. Nuclear staining and flow cytometry were carried out to further assess apoptosis. Mitochondrial membrane potential evaluation and Western blot analysis were performed to investigate the mechanism of peiminine-induced apoptosis. Peiminine reduced the viability of HepG2 cells in a time- and dose-dependent manner and had an IC ₅₀ of 4.58 μg/mL at 24h. Flow cytometry assessment indicated that peiminine markedly increased the cell number of apoptotic cells and the mitochondrial membrane potential dose-dependently in HepG2 cells. The results of Western blotting showed the expression of Bcl-2, procaspase-3, procaspase-8, procaspase-9, and PARP ₁ decreased in HepG2 cells treated with peiminine, while the expression of Bax, caspase-3, caspase-8, caspase-9, and cleaved PARP ₁ increased. The result suggest taht peiminine can induce apoptosis in human hepatocellular carcinoma HepG2 cells through both extrinsic and intrinsic apoptotic pathways.

Diacylglycerol kinase zeta (DGKZ) is associated with the pathogenesis of a variety of malignant diseases, but its biological function on acute myeloid leukemia (AML) has not been explored. This study was aimed to analyze apoptosis induced by Knockdown of DGKZ and its mechanism in human acute myeloid leukemia HL-60 cells.In the present study qRT-PCR was used to detect the expression of DGKZ in HL-60, THP-1, K562, H9, Jurkat and CD34 cell lines. DGKZ-shRNA lentiviral vector was established and used to infect acute myeloid leukemia HL-60 cells. Cell Counting Kit-8 (CCK-8) assay was used to determine the viability of HL-60 cells DGKZ knocked down. Apoptosis and cell cycle phase of HL-60 cells after DGKZ knockdown were evaluated by flow cytometry. Western blot analysis was performed to investigated the protein expression related to apoptosis and cell cycle. Results showed DGKZ expression were stable and higher in Jurkat, HL-60, THP-1,K562 leukemia cells than those of H9 and CD34 cells. Compared with cells of the shCtrl group, DGKZ was markedly knocked down in cells which were transfected with lentivirus encoding shRNA of DGKZ in HL-60 cells. DGKZ knockdown significantly inhibited the proliferation and induced cycle arrest at the G2/M phase in HL-60 cells. Western blot results indicated the expressions of caspase-3, caspase-8, and survivin markedly increased in HL-60 cells after knockdown of DGKZ. The results suggest Knockdown of DGKZ can inhibit proliferation of acute myeloid leukemia HL-60 cell caused cell cycle arrest at the G2/M phase through caspases pathway.