首页 返回上一页

针对病种:乳腺癌

发表时间:2015年1月

发表国家:瑞士

登载刊物:细胞生理学和生物化学:国际实验细胞生理学,生物化学和药理学杂志

研究单位:中国广西省,桂林医科大学基础医学院

研究人员:陈建,林长荣,雍王,等

主要结论:与金雀异黄素相比,通过调节Akt信号通路和HOTAIR表达,胆碱毛蕊异黄酮可以有效地抑制乳腺癌的生长.

Cellular Physiology & Biochemistry International Journal of Experimental Cellular Physiology Biochemistry & Pharmacology, 2015, 35(2):722-728.

Calycosin and Genistein Induce Apoptosis by Inactivation of HOTAIR/p-Akt Signaling Pathway in Human Breast Cancer MCF-7 Cells

Jian Chen, Changrong Lin, Wang Yong, et al

School of Basic Medical Sciences, Guilin Medical University, Guilin, China

BACKGROUND:

Calycosin and genistein are the two main components of isoflavones. Previously, we reported that these compounds display antitumor activities in the breast cancer cell lines MCF-7 and T47D. In the present study, we investigated the mechanism of action of calycosin and genistein, and their respective efficacies as potential therapies for the treatment of breast carcinoma in the clinic.

METHODS:

MCF-7 cells were treated with calycosin or genistein. Cell proliferation and apoptosis were measured using CCK8 assay and Hoechst 33258. The expression level of phosphorylated Akt protein was determined by western blotting. Expression level of HOTAIR was quantified by real-time PCR.

RESULTS:

Both calycosin and genistein inhibited proliferation and induced apoptosis in MCF-7 breast cancer cells, especially after treatment with calycosin. Treatment of MCF-7 cells with calycosin or genistein resulted in decreased phosphorylation of Akt, and decreased expression of its downstream target, HOTAIR.

CONCLUSION:

Calycosin is more effective in inhibiting breast cancer growth in comparison with genistein, through its regulation of Akt signaling pathways and HOTAIR expression.

瑞士《细胞生理学和生物化学:国际实验细胞生理学,生物化学和药理学杂志》,20151

在人体乳腺癌 MCF-7 细胞中毛蕊异黄酮和金雀异黄素通过HOTAIR/p-Akt信号转导途径的失活诱导细胞凋亡

陈建,林长荣,雍王,等

中国广西省,桂林医科大学基础医学院

背景:

毛蕊异黄酮和金雀异黄素是异黄酮的两个主要成分。 以前,我们报道了这些化合物在乳腺癌细胞系MCF-7T47D中显示出抗肿瘤活性。 在本研究中,我们探究了毛蕊异黄酮和金雀异黄素作为临床治疗乳腺癌的潜在疗法的作用机制及其各自的功效。

方法:

用毛蕊异黄酮或金雀异黄素处理MCF-7细胞。 使用CCK8Hoechst 33258等方法测量细胞的增殖和凋亡。通过免疫印迹法测定磷酸化Akt蛋白的表达水平。 HOTAIR的表达水平通过实时PCR确定。

结果:

毛蕊异黄酮和金雀异黄素均抑制MCF-7乳腺癌细胞的增殖,诱导细胞凋亡,特别是用毛蕊异黄酮治疗后。 用毛蕊异黄酮或金雀异黄素处理MCF-7细胞导致Akt的磷酸化降低并降低其下游靶标HOTAIR的表达。

结论:

与金雀异黄素相比,通过调节Akt信号通路和HOTAIR表达,胆碱毛蕊异黄酮可以有效地抑制乳腺癌的生长。
 石家庄霹克医药科技有限公司 400-831-3116