文献类型：期刊文献

英文题名：Overexpression of MiR-633 Suppresses the Tumorigenicity of Gastric Cancer Cells and Induces Apoptosis by Targeting MAPK1

作者：Li, Hai-long[1,2,3];Song, Yao-hui[2];Du, Zheng-ping[2];Hu, Yong-hua[2,3];Wang, Zhuan-xiong[2];Chen, Xi[2];Lu, Xing-mei[4];Chen, Ying-xia[5];Duan, Yong-qiang[5];Zhu, Xiang-dong[5]

第一作者：李海龙

通信作者：Zhu, XD[1]

机构：[1]Gansu Univ Tradit Chinese Med, Affiliated Hosp, Dept Geriatr, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Clin Med Coll 1, Dept Internal Med, Lanzhou 730000, Peoples R China;[3]Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent &, Lanzhou 730000, Peoples R China;[4]Gansu Vocat Coll Hlth, Sch Basic Med, Lanzhou 730300, Peoples R China;[5]Ningxia Med Univ, Coll Tradit Chinese Med, Yinchuan 750004, Ningxia, Peoples R China

第一机构：甘肃中医药大学第二附属医院

通信机构：[1]corresponding author), Ningxia Med Univ, Coll Tradit Chinese Med, Yinchuan 750004, Ningxia, Peoples R China.

年份：2022

卷号：42

期号：5

起止页码：1033

外文期刊名：CURRENT MEDICAL SCIENCE

收录：;Scopus(收录号：2-s2.0-85140134436);WOS:【SCI-EXPANDED(收录号:WOS:000870107900004)】；

基金：The study was supported by grants from Natural Science Foundation of Gansu Province (No. 20JR5RA189 and No. 17JR5RA169), the Foundation of the fundamental scientific research funds for colleges and universities in Gansu Province [No. (2014) 63-15], and the National Natural Science Fundation of China (No. 81760830).

语种：英文

外文关键词：miR-633; gastric cancer; apoptosis; metastasis; mitogen-activated protein kinase 1

摘要：Objective MicroRNA (miRNA/miR)-633 is dysregulated in several types of cancers and is involved in tumorigenesis. However, the function and role of this miRNA in gastric cancer (GC) are not fully understood. The aim of the present study was to evaluate miR-633 expression in GC cell lines and in GC tissue vs. adjacent normal tissue, and to determine its association with clinicopathological data. This work was extended to investigate the effects of miR-633 overexpression on tumor cells in vitro. Methods Reverse transcription-quantitative PCR (RT-qPCR) was used to detect and compare the expression level of miR-633 in GC cells, as well as in GC and normal adjacent tissue samples. The clinical significance of miR-633 was also analyzed. MiR-633 lentivirus (LV-miR-633) and negative control lentivirus (LV-NC) were generated and used to transduce SGC-7901 and HGC-27 GC cells in order to analyze the effect of miR-633 on their phenotype. The effects of miR-633 overexpression on GC cell proliferation, apoptosis, migration and invasion were investigated. The target gene of miR-633 was predicted, then confirmed using a dual luciferase reporter gene assay, RT-qPCR and Western blotting. Results MiR-633 was significantly downregulated in GC cell lines, as well as in GC tissue compared with adjacent normal tissue. Moreover, miR-633 expression was associated with the tumor/node/metastasis (TNM) stage, invasion depth, Borrmann classification and lymph node metastasis (P<0.05). Compared with the LV-NC group, transduction with LV-miR-633 reduced the proliferation, the number of clones, the wound healing rate, the number of invading cells and the number of cells in the G(1) phase of the cell cycle (P<0.01). LV-miR-633 also increased the apoptosis rate (P<0.01). The expression level of mitogen-activated protein kinase (MAPK) 1, high-mobility group box 3 (HMGB3), claudin 1 (CLDN1) and MAPK13 were downregulated in LV-miR-633-transduced cells (P<0.01). The dual luciferase reporter assay confirmed that the 3 '-untranslated region of MAPK1 was the target site of miR-633 (P<0.01). Conclusion MiR-633 acts as a tumor suppressor in GC, and its expression level is associated with TNM stage, invasion depth, Borrmann type and lymph node metastasis. Overexpression of miR-633 inhibits the proliferation and migration of GC cells and induces apoptosis and cell cycle arrest at the in G(1) phase. In addition, miR-633 negatively regulates the expression of MAPK1, HMGB3, CLDN1 and MAPK13 and directly targets MAPK1.