Shuai Wang1, Xinyan Zhang2, Houfa Ning3, Senyi Dong3, Guangzhi Wang4, Ruimei Sun5. 1. Department of Radiotherapy, Affiliated Hospital of Weifang Medical University, No. 2428, Yuhe Road, Weifang, 261031, Shandong Province, China. 2. Department of Intervention, The Affiliated Weihai Second Municipal Hospital of Qingdao University, Weihai, 264200, China. 3. School of Medical Imaging, Weifang Medical University, No. 7166, Baotong West Street, Weifang, 261053, Shandong Province, China. 4. School of Medical Imaging, Weifang Medical University, No. 7166, Baotong West Street, Weifang, 261053, Shandong Province, China. wgzshwf@163.com. 5. Department of Radiotherapy, Affiliated Hospital of Weifang Medical University, No. 2428, Yuhe Road, Weifang, 261031, Shandong Province, China. sunruimei2012@126.com.
Abstract
PURPOSE: The essential action of B7 homolog 3 (B7-H3) in different diseases and cancers has been documented. We here focused on its role in breast cancer through the Raf/MEK/ERK axis regarding lung metastasis. METHODS: Expression pattern of B7-H3 was determined in breast cancer tissues and cells with its correlation with prognosis analyzed. Then, through transfection of lentivirus vector expressing B7-H3-shRNA, overexpression vector of B7-H3 (B7-H3-LV), U0126 (small molecule inhibitor of MEK), or PD98059 (small molecule inhibitor of ERK), the in vitro and in vivo effects of B7-H3 in breast cancer cell biological processes, and lung metastasis were analyzed in relation to the Raf/MEK/ERK axis. RESULTS: We discovered elevated B7-H3 in breast cancer and its elevation associated with poor prognosis. B7-H3 promoted the malignant properties of breast cancer cells, accompanied with increased N-cadherin and vimentin and reduced E-cadherin. Additionally, overexpression of B7-H3 accelerated the lung metastasis in breast cancer in vivo. All the above promoting action of B7-H3 was achieved through activation of the Raf/MEK/ERK signaling pathway. CONCLUSION: Taken together, B7-H3 can promote lung metastasis in breast cancer through activation of the Raf/MEK/ERK axis.
PURPOSE: The essential action of B7 homolog 3 (B7-H3) in different diseases and cancers has been documented. We here focused on its role in breast cancer through the Raf/MEK/ERK axis regarding lung metastasis. METHODS: Expression pattern of B7-H3 was determined in breast cancer tissues and cells with its correlation with prognosis analyzed. Then, through transfection of lentivirus vector expressing B7-H3-shRNA, overexpression vector of B7-H3 (B7-H3-LV), U0126 (small molecule inhibitor of MEK), or PD98059 (small molecule inhibitor of ERK), the in vitro and in vivo effects of B7-H3 in breast cancer cell biological processes, and lung metastasis were analyzed in relation to the Raf/MEK/ERK axis. RESULTS: We discovered elevated B7-H3 in breast cancer and its elevation associated with poor prognosis. B7-H3 promoted the malignant properties of breast cancer cells, accompanied with increased N-cadherin and vimentin and reduced E-cadherin. Additionally, overexpression of B7-H3 accelerated the lung metastasis in breast cancer in vivo. All the above promoting action of B7-H3 was achieved through activation of the Raf/MEK/ERK signaling pathway. CONCLUSION: Taken together, B7-H3 can promote lung metastasis in breast cancer through activation of the Raf/MEK/ERK axis.
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