Jiang Liangqian, Wang Yujuan, Liu Guoxiang, Liu Huihui, Zhu Feng, Ji Huanhuan, Li Bing
Department of Genetics and Cell Biology, Basic Medical College, Qingdao University, 308 Ningxia Road, Qingdao, 266071 China.
Cancer Cell Int. 2018 Jan 25;18:12. doi: 10.1186/s12935-018-0511-5. eCollection 2018.
Triple-negative breast cancer is a biological subtype of breast cancer, which is unresponsive to conventional chemotherapies and has a poor prognosis. C-Phycocyanin (C-PC), a marine natural purified from , has been investigated that has anti-cancer function. The mitogen activated protein kinase (MAPK) pathway plays a crucial role in the development and progression of cancer. Therefore, we would like to study the anti-cancer effects of C-phycocyanin in the treatment of triple-negative breast cancer, and explore the role of MAPK pathway in the anti-tumor effects of C-phycocyanin.
Cell proliferation, cell cycle, cell apoptosis and cell migration were explored in breast cancer MDA-MB-231 cell lines. AKT, MAPK and membrane death receptor signaling were evaluated in MDA-MB-231 cell lines.
Our study indicated that C-phycocyanin inhibited cell proliferation and reduced colony formation ability of MDA-MB-231 cells. Furthermore, C-phycocyanin induced cell cycle G0/G1 arrest by decreasing protein expression levels of Cyclin D1 and CDK-2 and increasing protein expression levels of p21 and p27. In addition, C-phycocyanin induced cell apoptotic by activating cell membrane surface death receptor pathway. Besides, C-phycocyanin down-regulated the protein expression levels of cyclooxygenase-2, and further inhibited MDA-MB-231 cells migration. We also found cell death induced by C-phycocyanin was carried through the MAPK signaling pathways. C-Phycocyanin was able to induce MDA-MB-231 cell apoptosis by activating p38 MAPK and JNK signaling pathways while inhibiting ERK pathway.
C-Phycocyanin exerted anti-cancer activity via the MAPK signaling pathway in MDA-MB-231 cells.
三阴性乳腺癌是乳腺癌的一种生物学亚型,对传统化疗无反应且预后较差。藻蓝蛋白(C-PC)是一种从海洋中提纯的天然物质,已被研究证实具有抗癌功能。丝裂原活化蛋白激酶(MAPK)通路在癌症的发生和发展中起关键作用。因此,我们旨在研究藻蓝蛋白在治疗三阴性乳腺癌中的抗癌作用,并探讨MAPK通路在藻蓝蛋白抗肿瘤作用中的作用。
在乳腺癌MDA-MB-231细胞系中研究细胞增殖、细胞周期、细胞凋亡和细胞迁移情况。在MDA-MB-231细胞系中评估AKT、MAPK和膜死亡受体信号。
我们的研究表明,藻蓝蛋白抑制MDA-MB-231细胞的增殖并降低其集落形成能力。此外,藻蓝蛋白通过降低细胞周期蛋白D1和细胞周期蛋白依赖性激酶-2的蛋白表达水平以及增加p21和p27的蛋白表达水平,诱导细胞周期G0/G1期阻滞。此外,藻蓝蛋白通过激活细胞膜表面死亡受体途径诱导细胞凋亡。此外,藻蓝蛋白下调环氧化酶-2的蛋白表达水平,并进一步抑制MDA-MB-231细胞迁移。我们还发现藻蓝蛋白诱导的细胞死亡是通过MAPK信号通路实现的。藻蓝蛋白能够通过激活p38 MAPK和JNK信号通路同时抑制ERK通路来诱导MDA-MB-231细胞凋亡。
藻蓝蛋白通过MAPK信号通路在MDA-MB-231细胞中发挥抗癌活性。