COL11A1 is Downregulated by miR-339-5p and Promotes Colon Carcinoma Progression

IF 2.7 4区 医学 Q2 Medicine Canadian Journal of Gastroenterology and Hepatology Pub Date : 2022-05-28 DOI:10.1155/2022/8116990
Weizhi Liu, Ke Meng
{"title":"COL11A1 is Downregulated by miR-339-5p and Promotes Colon Carcinoma Progression","authors":"Weizhi Liu, Ke Meng","doi":"10.1155/2022/8116990","DOIUrl":null,"url":null,"abstract":"The roles of COL11A1 in cancer have been increasingly considered, but the understandings of the effects of COL11A1 on colon carcinoma progress are much limited yet. qRT-PCR and Western blot were utilized to evaluate COL11A1 expression at mRNA and protein levels, respectively, in colon carcinoma cell lines. Afterward, the tumorigenesis biological effects of COL11A1 were examined by CCK-8, colony formation, Transwell, and wound healing methods. Moreover, upstream miRNAs containing the binding sites with COL11A1 were predicted by the bioinformatics methods. The interplay between COL11A1 and miR-339-5p was identified by a dual-luciferase assay. COL11A1 expression was prominently upregulated in colon carcinoma cell lines relative to that in normal human colon mucosal epithelial cell lines, and it was related to tumor stages. The outcomes of in-vitro experiments suggested that interfering with COL11A1 remarkably repressed the malignant behaviors of SW480 and SW620 cells. MiR-339-5p was markedly lowly expressed in colon carcinoma cell lines. Furthermore, miR-339-5p directly targeted and negatively regulated COL11A1 expression. COL11A1 upregulation promoted colon carcinoma cell functions, while overexpressing miR-339-5p evidently attenuated the promotion. These results proved the modulation of the miR-339-5p/COL11A1 axis in colon carcinoma cells, and miR-339-5p repressed colon carcinoma progression via COL11A1 downregulation. These results offer new underlying targets for the accurate therapy of colon carcinoma patients.","PeriodicalId":48755,"journal":{"name":"Canadian Journal of Gastroenterology and Hepatology","volume":"46 1","pages":""},"PeriodicalIF":2.7000,"publicationDate":"2022-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Canadian Journal of Gastroenterology and Hepatology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/2022/8116990","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 2

Abstract

The roles of COL11A1 in cancer have been increasingly considered, but the understandings of the effects of COL11A1 on colon carcinoma progress are much limited yet. qRT-PCR and Western blot were utilized to evaluate COL11A1 expression at mRNA and protein levels, respectively, in colon carcinoma cell lines. Afterward, the tumorigenesis biological effects of COL11A1 were examined by CCK-8, colony formation, Transwell, and wound healing methods. Moreover, upstream miRNAs containing the binding sites with COL11A1 were predicted by the bioinformatics methods. The interplay between COL11A1 and miR-339-5p was identified by a dual-luciferase assay. COL11A1 expression was prominently upregulated in colon carcinoma cell lines relative to that in normal human colon mucosal epithelial cell lines, and it was related to tumor stages. The outcomes of in-vitro experiments suggested that interfering with COL11A1 remarkably repressed the malignant behaviors of SW480 and SW620 cells. MiR-339-5p was markedly lowly expressed in colon carcinoma cell lines. Furthermore, miR-339-5p directly targeted and negatively regulated COL11A1 expression. COL11A1 upregulation promoted colon carcinoma cell functions, while overexpressing miR-339-5p evidently attenuated the promotion. These results proved the modulation of the miR-339-5p/COL11A1 axis in colon carcinoma cells, and miR-339-5p repressed colon carcinoma progression via COL11A1 downregulation. These results offer new underlying targets for the accurate therapy of colon carcinoma patients.
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
COL11A1被miR-339-5p下调并促进结肠癌进展
COL11A1在癌症中的作用已被越来越多地考虑,但对COL11A1在结肠癌进展中的作用的理解还很有限。采用qRT-PCR和Western blot分别在mRNA和蛋白水平上检测COL11A1在结肠癌细胞系中的表达。随后,采用CCK-8法、菌落形成法、Transwell法和创面愈合法检测COL11A1的肿瘤发生生物学效应。此外,通过生物信息学方法预测了含有COL11A1结合位点的上游mirna。COL11A1和miR-339-5p之间的相互作用是通过双荧光素酶测定确定的。COL11A1在结肠癌细胞系中的表达较正常人结肠粘膜上皮细胞系显著上调,且与肿瘤分期有关。体外实验结果表明,干扰COL11A1可显著抑制SW480和SW620细胞的恶性行为。MiR-339-5p在结肠癌细胞系中显著低表达。此外,miR-339-5p直接靶向并负调控COL11A1的表达。COL11A1上调可促进结肠癌细胞功能,而过表达miR-339-5p可明显减弱这种促进作用。这些结果证明了miR-339-5p/COL11A1轴在结肠癌细胞中的调节作用,miR-339-5p通过下调COL11A1抑制结肠癌的进展。这些结果为结肠癌患者的精准治疗提供了新的潜在靶点。
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
CiteScore
4.80
自引率
0.00%
发文量
0
审稿时长
37 weeks
期刊介绍: Canadian Journal of Gastroenterology and Hepatology is a peer-reviewed, open access journal that publishes original research articles, review articles, and clinical studies in all areas of gastroenterology and liver disease - medicine and surgery. The Canadian Journal of Gastroenterology and Hepatology is sponsored by the Canadian Association of Gastroenterology and the Canadian Association for the Study of the Liver.
期刊最新文献
Acute Variceal Hemorrhage in Germany-A Nationwide Study of 65,357 Hospitalized Cases: Variceal Hemorrhage in Germany. The Predictive Value of Time-Varying Noninvasive Scores on Long-Term Prognosis of NAFLD in South Korea. Feasibility and Acceptability of Antenatal Hepatitis C Screening: A Pilot Study. Primary Care Support Tools for Digestive Health Care: A Mixed Method Study. Long-Term Treatment with Bulevirtide in Patients with Chronic Hepatitis D and Advanced Chronic Liver Disease.
×
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