文献类型：期刊文献

英文题名：In Vitro and In Vivo Study on the Effect of Lysosome-associated Protein Transmembrane 4 Beta on the Progression of Breast Cancer

作者：Tao, Deyou[1];Liang, Junqing[2];Pan, Yihong[3];Zhou, Yanting[4];Feng, Ying[4];Zhang, Lin[4];Xu, Jingjing[4];Wang, Hui[4];He, Ping[4];Yao, Jie[4];Zhao, Yang[4];Ning, Qinjie[4];Wang, Wen[4];Jiang, Wei[4];Zheng, Jing[4];Wu, Xia[4]

机构：[1]Taizhou Enze Med Grp, Enze Hosp, Dept Oncol Surg, Luqiao, Zhejiang, Peoples R China;[2]Inner Mongolia Med Univ, Affiliated Peoples Hosp, Hohhot, Inner Mongolia, Peoples R China;[3]Gynecol Taizhou Enze Med Ctr Grp Enze Hosp, Taizhou, Zhejiang, Peoples R China;[4]East China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab New Drug Design, 130 Meilong Rd, Shanghai 200237, Peoples R China

年份：2019

卷号：22

期号：3

起止页码：375

外文期刊名：JOURNAL OF BREAST CANCER

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000488290200003)】；

基金：This study was funded by the National Natural Science Foundation of China (grant No. 31300904), the International Postdoctoral Exchange Fellowship Program (No. 20130018), and Higher Educational Scientific Research Projects of Inner Mongolia Autonomous Region (No. NJZZ098).

语种：英文

外文关键词：Breast neoplasms; Disease progression; LAPTM4B protein; human; MCF-7 cells

摘要：Purpose: Although the effect of lysosome-associated protein transmembrane 4 beta (LAPTM4B) on the proliferation, migration, and invasion of breast cancer (BC) cells has already been studied, its specific role in BC progression is still elusive. Here, we evaluated the effect of different levels of LAPTM4B expression on the proliferation, invasion, adhesion, and tumor formation abilities of BC cells in vitro, as well as on breast tumor progression in vivo. Methods: We investigated the influence of LAPTM4B expression on MCF-7 cell proliferation, invasion, adhesion, and tube formation abilities in vitro through its overexpression or knockdown and on breast tumor progression in vivo. Results: Cell growth curves and colony formation assays showed that LAPTM4B promoted the proliferation of breast tumor cells. Cell cycle analysis results revealed that LAPTM4B promoted the entry of cells from the G1 into the S phase. Transwell invasion and cell extracellular matrix adhesion assays showed that LAPTM4B overexpression increased the invasion and adhesion capabilities of MCF-7 cells. More branches were observed in MCF-7 cells overexpressing LAPTM4B under an electron microscope. In comparison with LAPTM4B overexpression, LAPTM4B knockdown decreased the expression of vascular endothelial growth factor-A and significantly inhibited the vasculogenic tube formation ability of tumors. These results were also verified with western blot analysis. Conclusion: LAPTM4B promoted the proliferation of MCF-7 cells through the downregulation of p21 (WAF1/CIP1) and caspase-3, and induced cell invasion, adhesion, and angiogenesis through the upregulation of hypoxia-inducible factor 1 alpha, matrix metalloproteinase 2 (MMP2), and MMP9 expression. This specific role deems LAPTM4B as a potential therapeutic target for BC treatment.