期刊
BIOMEDICINE & PHARMACOTHERAPY
卷 103, 期 -, 页码 1002-1011出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2018.04.052
关键词
Coptisine; Hepatocellular carcinoma; microRNA-122; Anti-cancer; Proliferation; Migration; Apoptosis
资金
- National Key Research and Development Program of China [2017YFC1702605, 2017YFC1702606, 2017YFD0501504]
- Special Program for Common and Key Technological Innovations of Key Industries in Chongqing [cstc2016zdcy-ztzx10001]
- Industrial Technology System Program for Traditional Chinese Herbs of Chongqing Municipal Agricultural Commission [2017[5]]
- Construction Project of Key subjects of Traditional Chinese Medicine of the State Administration of Traditional Chinese Medicine of the People's Republic of China
- County University cooperation Innovation Funds of Southwest University [SZ201703, HZ201601]
With increasing incidence and mortality, hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. In this study, microRNA-122 (miR-122) mimics and relevant control oligonucleotides were transfected into HepG2 cells in vitro, followed by coptisine (COP) and sorafenib treatments. Cell proliferation, migration, and apoptosis were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay, wound-healing assay, Hoechst 33258 staining and flow cytometry, respectively. Histopathology and miR-122 were analyzed by haemotoxylin and eosin (H&E) staining and real-time RT-PCR, respectively; whereas, the relevant protein expressions were detected by western blot. In vivo, COP enhanced the expression of miR-122 by 160% compared to control in male BALB/c nude mice; COP not only protected the liver morphology but also showed a significant anti-cancer effect. Further, there was no remarkable difference between the tumor weights in the COP and sorafenib groups, but there was a striking difference to the tumor control group (p < 0.05). Hence, COP inhibited the proliferation, migration and promoted apoptosis of HCC cells; moreover, it inhibited the tumor growth in nude mice by up-regulating the expression of miR-122.
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