Premium
TYMSOS drives the proliferation, migration, and invasion of gastric cancer cells by regulating ZNF703 via sponging miR‐4739
Author(s) -
Gu Yulan,
Wan Chuandan,
Zhou Guoqiang,
Zhu Jinlian,
Shi Zhiliang,
Zhuang Zhixiang
Publication year - 2021
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11610
Subject(s) - cell growth , flow cytometry , microbiology and biotechnology , apoptosis , biology , cancer cell , chemistry , cell migration , cell , cancer research , cancer , biochemistry , genetics
Gastric cancer (GC) is a kind of malignancy originating from the epithelium of gastric mucosa. Long noncoding RNAs (lncRNAs) are tightly related to the GC progression. Herein, our research was meant to investigate a novel lncRNA thymidylate synthetase opposite strand ( TYMSOS ) in GC. Quantitative real‐time polymerase chain reaction was used to analyze TYMSOS expression in GC cells. 5‐Ethynyl‐2ʹ‐deoxyuridine, flow cytometry analysis, and transwell assay detected the influence of TYMSOS on GC cell proliferation, apoptosis, migration, and invasion. Subcellular fractionation and fluorescent in situ hybridization assays determined the cellular localization of TYMSOS in GC cells. Bioinformatics programs, RNA‐binding protein immunoprecipitation, RNA pull‐down, and luciferase reporter assays measured the molecular interplays of TYMSOS in GC cells. In brief, TYMSOS was highly expressed in GC cells, and TYMSOS silence inhibited GC cell proliferation, migration, and invasion while elevating cell apoptosis. Functionally, TYMSOS functioned as a competing endogenous RNA to posttranscriptionally modulate GC progression. TYMSOS interacted with miR‐4739 to regulate its target gene zinc finger protein 703 . Collectively, our study proved the tumor‐promoting role of TYMSOS in GC cells, which might offer the utility value for GC treatment.