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The cellular apoptosis susceptibility (CSE1L) gene has been demonstrated to regulate multiple cellular mechanisms including the mitotic spindle check point as well as proliferation and apoptosis. However, the importance of CSE1L in human colon cancer is largely unknown. In the present study, we examined expression levels of CSE1L mRNA by semiquantitative RT-PCR. A lentivirus-mediated small interfering RNA (siRNA) was used to knock down CSE1L expression in the human colon cancer cell line RKO. Changes in CSE1L target gene expression were determined by RT-PCR. Cell proliferation was examined by a high content screening assay. In vitro tumorigenesis was measured by colony-formation assay. Cell cycle distribution and apoptosis were detected by flow cytometric analysis. We found CSE1L mRNA to be expressed in human colon cancer cells. Using a lentivirus based RNAi approach, CSE1L expression was significantly inhibited in RKO cells, causing cell cycle arrest in the G2/M and S phases and a delay in cell proliferation, as well as induction of apoptosis and an inhibition of colony growth capacity. Collectively, the results suggest that silencing of CSE1L may be a potential therapeutic approach for colon cancer.

Three new ruthenium(II) polypyridyl complexes [Ru(bpy)(2)(BHIP)](2+) 1, [Ru(phen)(2)(BHIP)](2+) 2, and [Ru(dip)(2)(BHIP)](2+) 3 were synthesized and characterized. The cytotoxicity of the three complexes was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis induced by the complexes was studied by cell morphology and flow cytometry. The results showed that the percentage of apoptotic cells is 7.19%, 75.58%, and 3.51% in the presence of complexes 1, 2, and 3, respectively. The cellular uptakes were also performed and the results indicated that complexes 1, 2, and 3 can enter into the cytoplasm and also into the nucleus. The studies on antiproliferative mechanism showed the induction of S-phase arrest by complexes 1, 2, and 3. DNA-binding constants of these complexes with calf thymus DNA (CT-DNA) were determined to be 1.07 (± 0.47) × 10(5) M(-1) (s = 2.04), 1.21 (± 0.32) × 10(5) M(-1) (s = 1.88), and 2.75 (± 0.27) × 10(5) M(-1) (s = 2.17), respectively. Upon irradiation at 365 nm, complexes 1, 2, and 3 can induce cleavage of pBR322 DNA.

Objective: To explore the molecular mechanism of apoptosis induced by enterovirus 71 (EV71) infection., Methods: The effects of EV71 on Rhabdomyosarcoma (RD) cell viability were detected by CCK8 assay. EV71-induced apoptosis on RD cells were detected by Hoechst 33342 staining and Western blot targeting Caspase 3, 8 and PARP. Bax conformational change was detected by immunoprecipitation with Bax 6A7 antibody., Results: EV71 decreased the viability of RD cells and induces the activation of Caspase 3, 8 and PARP. Bax expression increases in RD cells after EV71 infection, and Bax conformational change also can be detected after EV71 infection., Conclusion: Our study reveals that EV71 induces Caspase-dependent apoptosis by Bax conformational change.

Pyroptosis is a newly discovered form of programmed cell death mediated by the gasdermin protein, that is accompanied by inflammation and immune response. A growing body of evidence suggests that pyroptosis is closely related to cancer, and it is becoming a new cancer research topic. Studies have suggested that different cancer cells activate pyroptosis in different ways and that the effects of pyroptosis vary in different cancer backgrounds. In this article, we briefly introduce the definition, characteristics, and activation pathways of pyroptosis. Then we review the complex effects of pyroptosis on cancer development, which generally include inhibition of cancer cell viability, impacts on the invasion and migration of cancer cells, improvement of antitumor immunity, and enhancement of chemotherapy sensitivity. We also discuss drugs and compounds that can induce pyroptosis, as well as the interaction between pyroptosis and apoptosis. Elucidating the mechanisms of the complex effects of pyroptosis is likely to pave the way for therapeutic approaches for cancer in the future. [ABSTRACT FROM AUTHOR]

Two new ruthenium(II) complexes, [Ru(dmp)2(BHIP)]2+ (1) and [Ru(dmb)2(BHIP)]2+ (2), were synthesized and characterized by elemental analysis, ESI-MS, and 1H NMR. DNA-binding constants of these complexes with calf-thymus DNA (ct-DNA) were determined to be 2.09 (±0.18) × 104 (mol L−1)−1 (s = 2.58) and 1.48 (±0.17) × 105 (mol L−1)−1 (s = 1.57), respectively. Viscosity measurements show that 1 and 2 interact with ct-DNA by intercalation. Upon irradiation at 365 nm, 1 and 2 induce cleavage of pBR322 DNA. The cytotoxicity of these complexes was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The apoptosis induced by the complexes was studied by flow cytometry. The results of the cell cycle arrest show that 2 can inhibit the proliferation of BEL-7402 cells in the G0/G1 phase. [ABSTRACT FROM PUBLISHER]

Radiation has large influence on the cytotoxicity, apoptosis and cell cycle arrest. The bioactivity of ruthenium(II) complex [Ru(dmb) 2 (DBHIP)](ClO 4 ) 2 ( Ru1 ) (DBHIP = 2-(3,5-dibromo-4-hydroxylphenyl)imidazo[4,5-f][1,10]phenanthroline) was investigated in the absence and presence of radiation. The cytotoxicity of Ru1 against MG-63 cells was evaluated by CCK-8 method. Ru1 shows high cytotoxicity upon radiation. Radiation can enhance the cytotoxicity of Ru1 on MG-63 cells. The apoptosis was studied by Hoechst 33258 staining method and flow cytometry. The reactive oxygen species, mitochondrial membrane potential, cell cycle arrest and western blot analysis were investigated in detail. The complex induces the apoptosis in MG-63 cells through ROS-mediated mitochondrial dysfunction pathway. [ABSTRACT FROM AUTHOR]