Depletion of SENP1 suppresses the proliferation and invasion of triple-negative breast cancer cells

被引:32
|
作者
Wang, Zhonghua [1 ,2 ]
Jin, Jia [1 ,2 ]
Zhan, Jian [1 ,2 ]
Wang, Leiping [1 ,2 ]
Cao, Jun [1 ,2 ]
机构
[1] Fudan Univ, Shanghai Canc Ctr, Dept Med Oncol, 270 Dong Rd, Shanghai 200032, Peoples R China
[2] Fudan Univ, Shanghai Med Coll, Dept Oncol, Shanghai 200032, Peoples R China
关键词
triple-negative breast cancer; SUMO-specific protease 1; proliferation; invasion; therapeutic target; SUMO-SPECIFIC PROTEASE-1; PROSTATE-CANCER; SIGNALING PATHWAY; EXPRESSION; GROWTH; TUMORS; MMP-9; RADIOSENSITIZATION; SUMOYLATION; METASTASIS;
D O I
10.3892/or.2016.5036
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
To investigate the roles of SUMO-specific protease 1 (SENP1) in triple-negative breast cancer (TNBC), we detected the expression level of SENP1 in the clinical samples of TNBC and non-TNBC patients by using immunohistochemical staining, qRT-PCR, and western blotting. We found that SENP1 was highly expressed in the TNBC tissues compared with the normal breast tissues, as well as non-TNBC tissues. Next, we constructed the si-SENP1-transfected TNBC cell lines for further biological function investigation. Then a xenograft model of nude mice was constructed to confirm the roles of SENP1 in TNBC formation and metastasis. According to our results, deficiency of SENP1 significantly represses the proliferation, invasion, migration, and colony formation of TNBC cells through blocking the cell cycle and regulating the expression of cyclin-dependent kinases (CDKs) p21 and p27, as well as MMP9. Furthermore, in vivo experiments revealed that depletion of SENP1 remarkably inhibits the tumor volume, lung metastatis and the expression of p21, p27, MMP9, and Ki67. Taken together, this study elucidated that SENP1 is essential for TNBC cell proliferation and migration in vitro, as well as tumor formation and metastasis in vivo, indicating that SENP1 is a potential therapeutic target for TNBC treatment.
引用
收藏
页码:2071 / 2078
页数:8
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