RETRACTED: MiR-132 enhances proliferation and migration of HaCaT cells by targeting TIMP3 (Retracted article. See vol. 11, pg. 5002, 2021)

被引:3
|
作者
Jiang, Lina [1 ]
Jiang, Yizhou [2 ]
Ji, Xiaohui [3 ]
Li, Jiangtao [4 ]
Zhai, Ximei [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Plast Surg, 1 East Jianshe Rd, Zhengzhou 450052, Henan, Peoples R China
[2] Fudan Univ, Shanghai Canc Ctr, Dept Breast Surg, Shanghai 200032, Peoples R China
[3] Dept Pathol, Beijing, Peoples R China
[4] Peoples Hosp Zhengzhou, Dept Breast Surg, Zhengzhou 450003, Henan, Peoples R China
基金
中国国家自然科学基金;
关键词
GROWTH-FACTOR; EXPRESSION; KERATINOCYTES; REEPITHILIALIZATION; METALLOPROTEINASES; MICRORNA-132; TRANSITION; MIR-21;
D O I
10.1039/c8ra10552a
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
MicroRNAs (miRNAs) are involved in multiple skin pathologies, including wound healing. Here, we explored the detailed role and molecular mechanism of miR-132 on HaCaT cells proliferation and migration. qRT-PCR assay was used to assess miR-132 expression and Western blot analysis was performed to detect inhibitor of matrix metalloproteinase-3 (TIMP3) level in HaCaT cells and normal human epidermal keratinocytes (NHEK) under transforming growth factor beta 1 (TGF-beta 1) treatment. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were employed to confirm the endogenous interaction between miR-132 and TIMP3. Cell proliferation ability was determined by MTT assay and the migration capacity was evaluated by transwell assay. TGF-beta 1 treatment resulted in a increase of miR-132 expression and a decrease of TIMP3 level in HaCaT cells and NHEK cells. The proliferation and migration abilities of TGF-beta 1-treated HaCaT cells were promoted by miR-132 upregulation, while them were inhibited by TIMP3 overexpression. Moreover, TIMP3 was a direct target of miR-132. MiR-132-mediated pro-proliferation and pro-migration effects were antagonized by TIMP3 in HaCaT cells under TGF-beta 1 treatment. Our data supported that miR-132 promoted the proliferation and migration of HaCaT cells at least partly by targeting TIMP3, highlighting miR-132 as a potential therapeutic strategy of wound healing.
引用
收藏
页码:21125 / 21133
页数:9
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