Cellular Physiology & Biochemistry International Journal of Experimental Cellular Physiology Biochemistry & Pharmacology, 2015, 35(5):2069-2077.

Genistein Inhibits Human Colorectal Cancer Growth and Suppresses MiR-95, Akt and SGK1

Jian Qin, Jia Xin Chen, Zhou Zhu, et al

Department of Radiation Oncology of Clinical Cancer Center, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China

Genistein, a major isoflavonoid isolated from dietary soybean, has been shown to suppress the growth of several cancers through modulation of various pathways. However, the molecular mechanisms by which genistein elicit its effects on colorectal cancer (CRC) cells have not been fully elucidated. In this study, we aimed to investigate the anti-tumor activities of genistein on CRC and its potential mechanism.Effects of genistein on the cell proliferation were tested in HCT-116 cells by MTT assay, and apoptosis was measured by Flow cytometry. Real-time PCR was also used to evaluate the regulation of genistein on miR-95, Akt and SGK1 expression. The protein levels of total Akt (T-Akt), and phosphorylated Akt (P-Akt) were assessed by western blot. A nude mice xenograft model was employed to determine whether genistein could have an anti-tumor effect on CRC in vivo.We found that treatment of HCT-116 cells with genistein caused an inhibition of cell proliferation and induction of apoptosis. Meanwhile, genistein down-regulated the mRNA expression of Akt, SGK1 and miR-95, and inhibited the phosphorylation of Akt in HCT-116 cells. The experiment in vivo also showed that genistein significantly suppressed the growth of mouse xenograft tumor.This study demonstrates that genistein has an inhibitory effect on CRC involved in reducing miR-95, Akt and SGK1, offering novel insights into the mechanisms of genistein therapeutic actions.

《细胞生理学与生物化学实验细胞生理学生物化学及药理学，国际杂志》2015

金雀异黄素抑制人体大肠癌生长和抑制因子 MiR-95、 Akt 和 SGK1

秦建，陈佳欣，朱州，等

临床癌症中心，广西壮族自治区人民医院，放疗科

染料木黄酮是从膳食大豆分离的主要异黄酮类化合物，已经显示通过调节各种途径抑制几种癌症的生长。然而，染料木黄酮引起其对结肠直肠癌（CRC）细胞的影响的分子机制尚未完全阐明。本研究旨在探讨染料木黄酮对CRC的抗肿瘤活性及其潜在机制。通过MTT法检测染料木素对HCT-116细胞增殖的影响，采用流式细胞仪检测细胞凋亡情况。还使用实时PCR来评价染料木黄酮对miR-95，Akt和SGK1表达的调节。通过蛋白质印迹评估总Akt（T-Akt）和磷酸化Akt（P-Akt）的蛋白质水平。使用裸鼠异种移植模型来确定染料木黄酮是否可以在体内对CRC具有抗肿瘤作用。我们发现用染料木黄酮治疗HCT-116细胞增殖的抑制和细胞凋亡的诱导。同时，染料木素下调Akt，SGK1和miR-95的mRNA表达，并抑制HCT-116细胞中Akt的磷酸化。体内实验还表明，染料木黄酮显著抑制小鼠异种移植肿瘤的生长。本研究表明，染料木黄酮对涉及减少miR-95，Akt和SGK1的CRC具有抑制作用，为染料木黄酮治疗作用的机制提供了新的见解。