Research on Correlations of lncRNA ST7-AS1 with Progression and Therapeutic Targets of Esophageal Cancer.

IF 1.4 4区 医学 Q4 GASTROENTEROLOGY & HEPATOLOGY Turkish Journal of Gastroenterology Pub Date : 2024-12-16 DOI:10.5152/tjg.2024.24260
Xiao Lin, Sijia Sun, JiWen Zhang, Yan Cai, Quan Cheng
{"title":"Research on Correlations of lncRNA ST7-AS1 with Progression and Therapeutic Targets of Esophageal Cancer.","authors":"Xiao Lin, Sijia Sun, JiWen Zhang, Yan Cai, Quan Cheng","doi":"10.5152/tjg.2024.24260","DOIUrl":null,"url":null,"abstract":"<p><p>Esophageal cancer is a highly prevalent gastrointestinal tumor in China, resulting in a significant number of deaths annually. In this paper, we investigated the regulatory role and therapeutic potential of aberrant ST7-AS1 expression in esophageal cancer. The presence of ST7-AS1 in 125 esophageal cancer tissues was identified through RT-qPCR assays. The application of Kaplan-Meier to evaluate survival rates in patients with esophageal cancer. Cell activity was assessed by both CCK-8 and Transwell assays. The luciferase activity assay verified the association of ST7-AS1 with miR-4262. ST7-AS1 expression in esophageal cancer was noticeably overexpressed compared to the control group. Patients with upregulated ST7-AS1 had shorter survival rates. Silencing ST7-AS1 reduced the proliferation level of esophageal cancer cells, as did the migration and invasion levels. Mechanistically, ST7-AS1 acted as a sponge for miR-4262, affecting the progression of esophageal cancer. This was negatively correlated with ST7-AS1. Moreover, the miR-4262 inhibitor negated the inhibitory effect of silencing ST7-AS1 on cells. Knockdown of ST7-AS1 may alleviate tumor progression by targeting miR-4262, indicating that ST7-AS1 is anticipated to serve as a therapeutic biomarker for patients with esophageal cancer.</p>","PeriodicalId":51205,"journal":{"name":"Turkish Journal of Gastroenterology","volume":"1 1","pages":"82-88"},"PeriodicalIF":1.4000,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Turkish Journal of Gastroenterology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5152/tjg.2024.24260","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Esophageal cancer is a highly prevalent gastrointestinal tumor in China, resulting in a significant number of deaths annually. In this paper, we investigated the regulatory role and therapeutic potential of aberrant ST7-AS1 expression in esophageal cancer. The presence of ST7-AS1 in 125 esophageal cancer tissues was identified through RT-qPCR assays. The application of Kaplan-Meier to evaluate survival rates in patients with esophageal cancer. Cell activity was assessed by both CCK-8 and Transwell assays. The luciferase activity assay verified the association of ST7-AS1 with miR-4262. ST7-AS1 expression in esophageal cancer was noticeably overexpressed compared to the control group. Patients with upregulated ST7-AS1 had shorter survival rates. Silencing ST7-AS1 reduced the proliferation level of esophageal cancer cells, as did the migration and invasion levels. Mechanistically, ST7-AS1 acted as a sponge for miR-4262, affecting the progression of esophageal cancer. This was negatively correlated with ST7-AS1. Moreover, the miR-4262 inhibitor negated the inhibitory effect of silencing ST7-AS1 on cells. Knockdown of ST7-AS1 may alleviate tumor progression by targeting miR-4262, indicating that ST7-AS1 is anticipated to serve as a therapeutic biomarker for patients with esophageal cancer.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
lncRNA ST7-AS1与食管癌进展及治疗靶点的相关性研究
食管癌在中国是一种非常普遍的胃肠道肿瘤,每年导致大量死亡。在本文中,我们探讨了ST7-AS1异常表达在食管癌中的调控作用和治疗潜力。通过RT-qPCR检测125例食管癌组织中ST7-AS1的存在。应用Kaplan-Meier评价食管癌患者的生存率。通过CCK-8和Transwell检测细胞活性。荧光素酶活性测定证实了ST7-AS1与miR-4262的关联。ST7-AS1在食管癌组织中的表达明显过表达。ST7-AS1表达上调的患者生存率较短。沉默ST7-AS1可降低食管癌细胞的增殖水平、迁移和侵袭水平。在机制上,ST7-AS1作为miR-4262的海绵,影响食管癌的进展。这与ST7-AS1呈负相关。此外,miR-4262抑制剂否定了沉默ST7-AS1对细胞的抑制作用。敲低ST7-AS1可能通过靶向miR-4262来缓解肿瘤进展,这表明ST7-AS1有望作为食管癌患者的治疗性生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Turkish Journal of Gastroenterology
Turkish Journal of Gastroenterology 医学-胃肠肝病学
CiteScore
1.90
自引率
0.00%
发文量
127
审稿时长
6 months
期刊介绍: The Turkish Journal of Gastroenterology (Turk J Gastroenterol) is the double-blind peer-reviewed, open access, international publication organ of the Turkish Society of Gastroenterology. The journal is a bimonthly publication, published on January, March, May, July, September, November and its publication language is English. The Turkish Journal of Gastroenterology aims to publish international at the highest clinical and scientific level on original issues of gastroenterology and hepatology. The journal publishes original papers, review articles, case reports and letters to the editor on clinical and experimental gastroenterology and hepatology.
期刊最新文献
Tanshinone IIA Restrains Hepatocellular Carcinoma Progression by Regulating METTL3-Mediated m6A Modification of TRIB3 mRNA. IREB2 Knockdown Alleviates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease by TLR4/NF-κB Signaling Inactivation. A Rare Case of Thyroid Abscess Requiring Surgical Intervention. Metabolic and Hepatic Profiles of Non-Obese and Obese Metabolic Dysfunction-Associated Steatotic Liver Disease in Adolescents: The Role of FibroScan Parameters,Fibroblast Growth Factor-21, and Cytokeratin-18. Impact of Caudate Lobe Resection on Overall Survival and Liver Disease-Free Survival in Colorectal Liver Metastases: A Pilot Study.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1