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Retracted : MicroRNA‐133a inhibits gastric cancer cells growth, migration, and epithelial‐mesenchymal transition process by targeting presenilin 1
Author(s) -
Chen XinBo,
Li Wei,
Chu AiXia
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27403
Subject(s) - epithelial–mesenchymal transition , viability assay , vimentin , apoptosis , biology , cancer research , downregulation and upregulation , microrna , notch signaling pathway , cell migration , microbiology and biotechnology , chemistry , cell , signal transduction , immunology , biochemistry , immunohistochemistry , gene
Gastric cancer (GC) is one of the most common malignancies and a leading cause of cancer‐related death worldwide. Accumulating evidence reported that microRNA (miR)‐133a was involved in GC. This study aimed to investigate the function and mechanism of miR‐133a in the development and progression of GC. The expression of miR‐133a and presenilin 1 (PSEN1) in two GC cell lines, SGC‐7901 and BGC‐823, were inhibited and overexpressed by transient transfections. Thereafter, cell viability, migration, and apoptosis were measured by trypan blue exclusion assay, transwell migration assay, and flow cytometry assay, respectively. Dual‐luciferase reporter assay was conducted to verify whether PSEN1 was a direct target of miR‐133a. Furthermore, quantitative real‐time polymerase chain reaction and Western blot analysis were mainly performed to assess the expression changes of epithelial‐mesenchymal transition (EMT)‐associated proteins, apoptosis‐related proteins, and Notch pathway proteins. MiR‐133a inhibitor significantly increased cell viability and migration, while miR‐133a mimic decreased cell viability, migration, and induced apoptosis. miR‐133a suppression accelerated transforming growth factor‐β1 (TGF‐β1)‐induce EMT, as evidenced by upregulation of E‐cadherin, and downregulation of N‐cadherin, vimentin, and Slug. Of contrast, miR‐133a overexpression blocked TGF‐β1‐induce EMT by altering these factors. PSEN1 was a direct target of miR‐133a, and suppression of PSEN1 abolished the promoting functions of miR‐133 suppression on cell growth and metastasis. Moreover, PSEN1 inhibition decreased Notch 1, Notch 2, and Notch 3 protein expressions. This study demonstrates an antigrowth and antimetastasis role of miR‐133a in GC cells. Additionally, miR‐133a acts as a tumor suppressor may be via targeting PSEN1.