Rap2B promotes proliferation, migration and invasion of human breast cancer through calcium-related ERK1/2 signaling pathway

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作者
Jiehui Di
Hui Huang
Debao Qu
Juangjuan Tang
Wenjia Cao
Zheng Lu
Qian Cheng
Jing Yang
Jin Bai
Yanping Zhang
Junnian Zheng
机构
[1] Cancer Institute,Department of Oncology
[2] Xuzhou Medical College,Department of Radiation Oncology and Lineberger Comprehensive Cancer Center
[3] Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy,undefined
[4] Cancer Institute,undefined
[5] Xuzhou Medical College,undefined
[6] the People’s Hospital of Kaixian,undefined
[7] School of Medicine,undefined
[8] the University of North Carolina at Chapel Hill,undefined
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摘要
Rap2B, a member of GTP-binding proteins, is widely upregulated in many types of tumors and promotes migration and invasion of human suprarenal epithelioma. However, the function of Rap2B in breast cancer is unknown. Expression of Rap2B was examined in breast cancer cell lines and human normal breast cell line using Western blot analysis. Using the CCK-8 cell proliferation assay, cell cycle analysis and transwell migration assay, we also elucidated the role of Rap2B in breast cancer cell proliferation, migration and invasion. Results showed that the expression of Rap2B is higher in tumor cells than in normal cells. Flow cytometry and Western blot analysis revealed that Rap2B elevates the intracellular calcium level and further promotes extracellular signal-related kinase (ERK) 1/2 phosphorylation. By contrast, calcium chelator BAPTM/AM and MEK inhibitor (U0126) can reverse Rap2B-induced ERK1/2 phosphorylation. Furthermore, Rap2B knockdown inhibits cell proliferation, migration and invasion abilities via calcium related-ERK1/2 signaling. In addition, overexpression of Rap2B promotes cell proliferation, migration and invasion abilities, which could be neutralized by BAPTM/AM and U0126. Taken together, these findings shed light on Rap2B as a therapeutic target for breast cancer.
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