Knockdown of Chloride Channel-3 Inhibits Breast Cancer Growth In Vitro and In Vivo

Fang-Min Zhou; Yun-Ying Huang; Tian Tian; Xiao Yan Liu; Yong-Bo Tang

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자료유형: 학술저널

저자정보: Fang-Min Zhou (Zhongshan School of Medicine Sun Yat-sen University) Yun-Ying Huang (The Fifth Affiliated Hospital of Guangzhou Medical University) Tian Tian (Zhongshan School of Medicine Sun Yat-sen University) Xiao Yan Liu (The Sixth Affiliated Hospital of Sun Yat-sen University) Yong-Bo Tang (Zhongshan School of Medicine Sun Yat-sen University)

저널정보: 한국유방암학회 Journal of Breast Cancer Journal of Breast Cancer Vol.21 No.2

발행연도: 2018.1

수록면: 103 - 111 (9page)

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Purpose: Chloride channel-3 (ClC-3) is a member of the chloride channel family and plays a critical role in a variety of cellular activities. The aim of the present study is to explore the molecular mechanisms underlying the antitumor effect of silencing ClC-3 in breast cancer. Methods: Human breast cancer cell lines MDAMB- 231 and MCF-7 were used in the experiments. Messenger RNA and protein expression were examined by quantitative realtime polymerase chain reaction and western blot analysis. Cell proliferation was measured by the bromodeoxyuridine method, and the cell cycle was evaluated using fluorescence-activated cell sorting. Protein interaction in cells was analyzed by co-immunoprecipitation. Tumor tissues were stained with hematoxylin- eosin and tumor burden was measured using the Metamorph software. Results: Breast cancer tissues collected from patients showed an increase in ClC-3 expression. Knockdown of ClC-3 inhibited the secretion of insulin-like growth factor (IGF)-1, cell proliferation, and G1/S transition in breast cancer cells. In the mouse xenograft model of human breast carcinoma, tumor growth was significantly slower in animals injected with ClC- 3-deficient cells compared with the growth of normal human breast cancer cells. In addition, silencing of ClC-3 attenuated the expression of proliferating cell nuclear antigen, Ki-67, cyclin D1, and cyclin E, as well as the activation of extracellular signalregulated protein kinases (ERK) 1/2, both in vitro and in vivo. Conclusion: Together, our data suggest that upregulation of ClC- 3 by IGF-1 contributes to cell proliferation and tumor growth in breast cancer, and ClC-3 deficiency suppresses cell proliferation and tumor growth via the IGF/IGF receptor/ERK pathway.

참고문헌 (23)

참고문헌 신청

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