Inactivated Tianjin strain, a novel genotype of Sendai virus, induces apoptosis in HeLa, NCI-H446 and Hep3B cells

Abstract

The Sendai virus strain Tianjin is a novel genotype of the Sendai virus. In previous studies, ultraviolet-inactivated Sendai virus strain Tianjin (UV-Tianjin) demonstrated antitumor effects on human breast cancer cells. The aim of the present study was to investigate the in vitro antitumor effects of UV-Tianjin on the human cervical carcinoma HeLa, human small cell lung cancer NCI-H446 and human hepatocellular carcinoma Hep 3B cell lines, and the possible underlying mechanisms of these antitumor effects. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay revealed that UV-Tianjin treatment inhibited the proliferation of HeLa, NCI-H446 and Hep 3B cells in a dose- and time-dependent manner. Hoechst and Annexin V-fluorescein isothiocyanate/propidium iodide double staining indicated that UV-Tianjin induced dose-dependent apoptosis in all three cell lines with the most significant effect observed in the HeLa cell line. In the HeLa cell line, UV-Tianjin-induced apoptosis was further confirmed by the disruption of the mitochondria membrane potential and the activation of caspases, as demonstrated by fluorescent cationic dye and colorimetric assays, respectively. In addition, western blot analysis revealed that UV-Tianjin treatment resulted in significant upregulation of cytochrome c, apoptosis protease activating factor-1, Fas, Fas ligand and Fas-associated protein with death domain, and activated caspase-9, −8 and −3 in HeLa cells. Based on these results, it is hypothesized that UV-Tianjin exhibits anticancer activity in HeLa, NCI-H446 and Hep 3B cell lines via the induction of apoptosis. In conclusion, the results of the present study indicate that in the HeLa cell line, intrinsic and extrinsic apoptotic pathways may be involved in UV-Tianjin-induced apoptosis.

Inactivated Sendai virus strain Tianjin induces apoptosis and autophagy through reactive oxygen species production in osteosarcoma MG‐63 cells

“…UV-inactivated Sendai virus has been shown to have antitumor activity against a variety of human cancer types (Chen et al, 2016;Gao et al, 2014;Kawaguchi et al, 2009; L.Y. Shi et al, 2015;Nomura, Shimbo, Miyamoto, Fukuzawa & Kaneda, 2013).…”

“…Several mechanisms such as inducing apoptosis pathway or antitumor immune response have been proposed in various cancer cells with Sendai virus treatment (Fujihara, Kurooka, Miki, & Kaneda, ; Gao et al, ; Kawaguchi, Miyamoto, Inoue, & Kaneda, ; Nomura, Shimbo, Miyamoto, Fukuzawa & Kaneda, ). In our previous study, ultraviolet‐inactivated Sendai virus strain Tianjin (UV‐Tianjin) particles were prepared to ensure the safety of virus and have been demonstrated to possess anticancer activities in many types of tumor cells (Chen, Han, Wang, & Shi, ; L. Shi et al, , L.Y. Shi et al, ).…”

Bioactivity Studies of Hesperidin and XAV939

“…The combination of XAV939 and cisplatin exhibited a slightly more pronounced inhibition of cell viability at an increased dose of the XAV939 drug. 37 Moreover, the effect of the HSP drug on the proliferation of the MCF-7 cell line transfected with green fluorescence protein (GFP)/α-tubulin (MCF-7-GFP-Tubulin cells), androgen-independent prostate cancer cells (PC-3), and androgen-dependent lymph node carcinoma of the prostate (LNCaP) and human prostate (DU-145) cancer cells. 38 The results showed the inhibition of breast cancer cell line proliferation (MCF-7-GFP-Tubulin cells).…”

“…The results of that study showed that XAV939 inhibited the viability of NCI-H446 cells in a dose-dependent manner; however, cisplatin as a positive control inhibited NCI-H446 cell viability in a time- and dose-dependent manner. The combination of XAV939 and cisplatin exhibited a slightly more pronounced inhibition of cell viability at an increased dose of the XAV939 drug . Moreover, the effect of the HSP drug on the proliferation of the MCF-7 cell line transfected with green fluorescence protein (GFP)/α-tubulin (MCF-7-GFP-Tubulin cells), androgen-independent prostate cancer cells (PC-3), and androgen-dependent lymph node carcinoma of the prostate (LNCaP) and human prostate (DU-145) cancer cells .…”

Regulation of Oxidative Stress by Different Naturally Occurring Polyphenolic Compounds: An Emerging Anticancer Therapeutic Approach

“…Genistein is capable of inducing apoptosis in the human cervical cancer cell line (HeLa) by inducing activation of caspase-9 and caspase-3, and decreasing the mitochondrial membrane potential which in turn increases oxidative stress. Genistein is the mostly studied soy isoflavone which has been accepted as an anticancer agent by the United Stated National Cancer Institute (NCI) in 1995 [76]. Different studies suggest that genistein inhibits cancer cell proliferation and metastasis and induces DNA fragmentation.…”