Abstract
Objective: To explore the function of miR-34a in promotion of apoptosis by SYB.
Methods: In this study, the most effective concentration of SYB was determined by measuring cell proliferation. Relative miR-34a mRNA levels were detected by quantitative RT-PCR. Apoptosis was assessed using Annexin- V/PI assays, whereas protein levels of p53, caspase 3, caspase 9, caspase 8 and Bcl2 were evaluated by western blotting. Results: Minimum HepG2 cell growth was observed after 36h of exposure to 150 nmol/L SYB. miR-34a expression was highest 40min after the addition of SYB. SYB slightly decreased the abundance of Bcl-2, but increased the abundance of p53, caspase 3, caspase 9 and caspase 8. SYB failed to alter miR-34a expression when p53 was inhibited. Bcl-2 abundance remained low over time, whereas the abundance of caspase 3, caspase 9 and caspase 8 gradually increased. Inhibition of p53 promoted HepG2 cell growth in comparison with that of the control group. miR-34a was silenced to assess the role of miR-34a in the inhibitory effect of SYB on HepG2 cell growth. When p53 was silenced, protein abundance of Bcl2, caspase 3, caspase 8 and caspase 9 remained unchanged following the addition of SYB; moreover, HepG2 cell growth was increased. Conlusion: SYB represents a promising therapeutic approach for liver cancer patients.Anti-Cancer Agents in Medicinal Chemistry
Title:Regulation of Apoptosis by SYB in HepG2 Liver Cancer Cells is Mediated by the P53/Caspase 9 Axis
Volume: 17 Issue: 7
Author(s): Sharula and Zhongjun Wu*
Affiliation:
- Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016,China
Keywords: SYB, p53, Caspase 9, HepG2, miR-34a.
Abstract: Objective: To explore the function of miR-34a in promotion of apoptosis by SYB.
Methods: In this study, the most effective concentration of SYB was determined by measuring cell proliferation. Relative miR-34a mRNA levels were detected by quantitative RT-PCR. Apoptosis was assessed using Annexin- V/PI assays, whereas protein levels of p53, caspase 3, caspase 9, caspase 8 and Bcl2 were evaluated by western blotting. Results: Minimum HepG2 cell growth was observed after 36h of exposure to 150 nmol/L SYB. miR-34a expression was highest 40min after the addition of SYB. SYB slightly decreased the abundance of Bcl-2, but increased the abundance of p53, caspase 3, caspase 9 and caspase 8. SYB failed to alter miR-34a expression when p53 was inhibited. Bcl-2 abundance remained low over time, whereas the abundance of caspase 3, caspase 9 and caspase 8 gradually increased. Inhibition of p53 promoted HepG2 cell growth in comparison with that of the control group. miR-34a was silenced to assess the role of miR-34a in the inhibitory effect of SYB on HepG2 cell growth. When p53 was silenced, protein abundance of Bcl2, caspase 3, caspase 8 and caspase 9 remained unchanged following the addition of SYB; moreover, HepG2 cell growth was increased. Conlusion: SYB represents a promising therapeutic approach for liver cancer patients.Export Options
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Cite this article as:
Sharula and Wu Zhongjun*, Regulation of Apoptosis by SYB in HepG2 Liver Cancer Cells is Mediated by the P53/Caspase 9 Axis, Anti-Cancer Agents in Medicinal Chemistry 2017; 17 (7) . https://dx.doi.org/10.2174/1871520617666170327161433
DOI https://dx.doi.org/10.2174/1871520617666170327161433 |
Print ISSN 1871-5206 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5992 |
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