4.5 Article

B7 homolog 3 induces lung metastasis of breast cancer through Raf/MEK/ERK axis

Journal

BREAST CANCER RESEARCH AND TREATMENT
Volume 193, Issue 2, Pages 405-416

Publisher

SPRINGER
DOI: 10.1007/s10549-022-06520-8

Keywords

B7-H3; Raf; MEK; ERK; Breast cancer; Lung metastasis

Categories

Funding

  1. General Project of Shandong Provincial Natural Science Foundation [ZR2020MH242, ZR2020MH293]
  2. Department of Health of Shandong Province [2018WS068]

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This study discovered elevated levels of B7-H3 in breast cancer, which were associated with poor prognosis. 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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