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Receptor activator of NF-kB (RANK) expression in primary tumors associates with bone metastasis occurrence in breast cancer patients.在乳腺癌患者中，原发肿瘤中 NF-κB（RANK）受体的表达与骨转移的发生相关。
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C-Src通过激活ERK和Akt通路介导RANKL诱导的乳腺癌细胞迁移。

C-Src-mediated RANKL-induced breast cancer cell migration by activation of the ERK and Akt pathway.

作者信息

Zhang Lingyun, Teng Yuee, Zhang Ye, Liu Jing, Xu Ling, Qu Jinglei, Hou Kezuo, Yang Xianghong, Liu Yunpeng, Qu Xiujuan

机构信息

Department of Medical Oncology, the First Hospital of China Medical University, Shenyang 110001, P.R. China.

出版信息

Oncol Lett. 2012 Feb;3(2):395-400. doi: 10.3892/ol.2011.487. Epub 2011 Nov 16.

DOI:10.3892/ol.2011.487
PMID:22740919
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3362513/
Abstract

The receptor activator for nuclear factor κB ligand/receptor activator for nuclear factor κB (RANKL/RANK) pathway is critical for RANK-expressing cancer cells to home to bones, and c-Src is critical for cancer progression. The objective of this study was to explore the effect of c-Src in the RANKL/RANK pathway and migration activity in human breast cancer cells. Breast cancer cell lines MCF-7, MDA-MB-231 and BT-474 were obtained and cultured. Flow cytometry was used to examine RANK expression. The results showed that RANK was expressed in breast cancer cell lines MCF-7, MDA-MB-231 and BT-474, and soluble RANKL (sRANKL)-triggered migration of breast cancer cells by activating ERK1/2, Akt and c-Src. The sRANKL-induced migration was blocked with RANKL inhibitor osteoprotegerin (OPG), MEK inhibitor PD98059, PI3K inhibitor LY294002 and Src inhibitor PP2. Inhibition of c-Src function with PP2 blocked the activation of Akt and ERK1/2, resulting in the inhibition of RANKL-induced migration. In conclusion, RANKL was found to increase the migration of breast cancer cells by activating the c-Src-Akt and c-Src-ERK signaling pathways.

摘要

核因子κB配体受体激活剂/核因子κB受体激活剂（RANKL/RANK）信号通路对于表达RANK的癌细胞归巢至骨骼至关重要，而c-Src对于癌症进展至关重要。本研究的目的是探讨c-Src在RANKL/RANK信号通路中的作用以及对人乳腺癌细胞迁移活性的影响。获取并培养乳腺癌细胞系MCF-7、MDA-MB-231和BT-474。采用流式细胞术检测RANK表达。结果显示，RANK在乳腺癌细胞系MCF-7、MDA-MB-231和BT-474中表达，可溶性RANKL（sRANKL）通过激活ERK1/2、Akt和c-Src触发乳腺癌细胞迁移。sRANKL诱导的迁移被RANKL抑制剂骨保护素（OPG）、MEK抑制剂PD98059、PI3K抑制剂LY294002和Src抑制剂PP2阻断。用PP2抑制c-Src功能可阻断Akt和ERK1/2的激活，从而抑制RANKL诱导的迁移。总之，发现RANKL通过激活c-Src-Akt和c-Src-ERK信号通路增加乳腺癌细胞的迁移。