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作 者:Ming He Ye Qi Ze-Mao Zheng Min Sha Xiang Zhao Yu-Rao Chen Zheng-Hai Chen Rong-Yu Qian Juan Yao Zheng-Dong Yang
机构地区:[1]Department of Radiation Oncology,Huai’an Hospital of Huai’an,Huai’an 223299,Jiangsu Province,China [2]Department of Nursing,Huai’an Hospital of Huai’an,Huai’an 223299,Jiangsu Province,China [3]Institute of Clinical Medicine,Taizhou People's Hospital Affiliated of Nantong University of Medicine,Taizhou 225300,Zhejiang Province,China [4]Department of Thoracic Surgery,Huai’an Hospital of Huai’an,Huai’an 223299,Jiangsu Province,China
出 处:《World Journal of Gastrointestinal Oncology》2024年第10期4194-4208,共15页世界胃肠肿瘤学杂志(英文)
基 金:Supported by Innovative Team of Jiangsu Province,No.CXTDA2017042;Jiangsu Provincial Medical Youth Talent,No.QNRC2016508;In-Hospital Project of Taizhou People's Hospital,No.ZL201930.
摘 要:BACKGROUND The clinical effects and detailed roles of long non-coding RNA(LncRNA)steroid receptor RNA activator 1(SRA1)in esophageal squamous cell carcinoma(ESCC)remain ambiguous.In the present study,the complementary sites between lncRNA SRA1,miRNA-363-5p,and phospholysine phosphohistidine inorganic pyrophosphate phosphatase(LHPP)predicted via bioinformatics analysis stimulated us to hypothesize that miRNA-363-5p/LHPP axis might be required for SRA1-mediated ESCC progression.AIM To investigate the molecular events of SRA1 in the malignant behavior in ESCC.METHODS Thirty-eight ESCC tissues and paired adjacent normal tissues were acquired.SRA1 expression was detected in ESCC tissues and cell lines using quantitative reverse transcription-polymerase chain reaction.Cell counting Kit-8 assay,transwell invasion assay,glycolysis assay,and xenograft tumor model were performed to address the malignant biological behaviors of ESCC cells after the introduction of SRA1.The t-test and theχ2 test were used for comparison between groups.Survival curve analysis was performed using the Kaplan-Meier method.RESULTS SRA1 downregulation was identified in ESCC.ESCC patients exhibiting a low SRA1 expression faced shorter overall survival than those with a high SRA1 expression.The introduction of SRA1 inhibited cell proliferation,glucose uptake,and lactate production in ESCC.In vivo,the growth of ESCC was hindered by SRA1 overexpression.Then,SRA1 overexpresses the LHPP by inhibiting miRNA-363-5p.Lastly,the introduction of small interfering RNA si-LHPP or miRNA-363-5p mimic could abrogate the inhibition roles triggered by SRA1.CONCLUSION SRA1 inhibits the oncogenicity of ESCC via miRNA-363-5p/LHPP axis.The SRA1/miRNA-363-5p/LHPP pathway may be a therapeutic target for ESCC.
关 键 词:Steroid receptor RNA activator 1 Esophageal squamous cell carcinoma Phospholysine phosphohistidine inorganic pyrophosphate phosphatase Cancer therapy MicroRNA Long non-coding RNA
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