KIAA1429 promotes the malignancy of oral squamous cell carcinoma by regulating CA9 m6A methylation

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Jia Tu, Xiao Feng, Qingqing Cao, Yan Guan
{"title":"KIAA1429 promotes the malignancy of oral squamous cell carcinoma by regulating CA9 m6A methylation","authors":"Jia Tu, Xiao Feng, Qingqing Cao, Yan Guan","doi":"10.1007/s10616-024-00640-3","DOIUrl":null,"url":null,"abstract":"<p>KIAA1429 has been reported as a cancer regulator, but its role and mechanism in the progression of oral squamous cell carcinoma (OSCC) remain elusive. The objective of the present research was to figure out the effect of KIAA1429 regulated CA9 on the progression of OSCC. Using qRT-PCR and bioinformatics analysis, we studied the expression levels of KIAA1429 and CA9 in OSCC tissue samples. The functional roles of KIAA1429 and CA9 were assessed using transwell and CCK-8 assays. The regulation among KIAA1429 and CA9 was investigated using MeRIP and western blotting assays. In addition, the m6A level in OSCC was measured utilizing RNA m6A quantification. In OSCC, KIAA1429 and m6A levels were upregulated. We observed that KIAA1429 inhibition declined proliferation, migration, and invasion of OSCC cells and decreased cell growth in vivo. Furthermore, KIAA1429 serves as a crucial upstream regulator of CA9 in OSCC and upregulates CA9 expression through an m6A-dependent mechanism. We observed that CA9 was upregulated in OSCC samples and that low expression of KIAA1429 partially restored the enhanced malignant phenotype caused by CA9 overexpression. Overall, our findings suggest that KIAA1429 and CA9 act as pro-oncogenic factors in OSCC, with KIAA1429 promoting OSCC malignancy through m6A modification-dependent stabilization of CA9 transcripts, which represents a novel regulatory mechanism in OSCC.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s10616-024-00640-3","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 0

Abstract

KIAA1429 has been reported as a cancer regulator, but its role and mechanism in the progression of oral squamous cell carcinoma (OSCC) remain elusive. The objective of the present research was to figure out the effect of KIAA1429 regulated CA9 on the progression of OSCC. Using qRT-PCR and bioinformatics analysis, we studied the expression levels of KIAA1429 and CA9 in OSCC tissue samples. The functional roles of KIAA1429 and CA9 were assessed using transwell and CCK-8 assays. The regulation among KIAA1429 and CA9 was investigated using MeRIP and western blotting assays. In addition, the m6A level in OSCC was measured utilizing RNA m6A quantification. In OSCC, KIAA1429 and m6A levels were upregulated. We observed that KIAA1429 inhibition declined proliferation, migration, and invasion of OSCC cells and decreased cell growth in vivo. Furthermore, KIAA1429 serves as a crucial upstream regulator of CA9 in OSCC and upregulates CA9 expression through an m6A-dependent mechanism. We observed that CA9 was upregulated in OSCC samples and that low expression of KIAA1429 partially restored the enhanced malignant phenotype caused by CA9 overexpression. Overall, our findings suggest that KIAA1429 and CA9 act as pro-oncogenic factors in OSCC, with KIAA1429 promoting OSCC malignancy through m6A modification-dependent stabilization of CA9 transcripts, which represents a novel regulatory mechanism in OSCC.

Abstract Image

KIAA1429 通过调节 CA9 m6A 甲基化促进口腔鳞状细胞癌的恶性发展
据报道,KIAA1429是一种癌症调控因子,但它在口腔鳞状细胞癌(OSCC)进展过程中的作用和机制仍不明确。本研究的目的是弄清 KIAA1429 调控的 CA9 对 OSCC 进展的影响。通过qRT-PCR和生物信息学分析,我们研究了KIAA1429和CA9在OSCC组织样本中的表达水平。我们还利用转孔试验和CCK-8试验评估了KIAA1429和CA9的功能作用。通过MeRIP和Western印迹实验研究了KIAA1429和CA9之间的调控作用。此外,还利用 RNA m6A 定量法测定了 OSCC 中的 m6A 水平。在 OSCC 中,KIAA1429 和 m6A 的水平呈上调趋势。我们观察到,KIAA1429抑制剂可减少OSCC细胞的增殖、迁移和侵袭,并降低细胞在体内的生长。此外,KIAA1429是OSCC中CA9的重要上游调节因子,并通过m6A依赖性机制上调CA9的表达。我们观察到 CA9 在 OSCC 样本中上调,而 KIAA1429 的低表达部分恢复了 CA9 过表达导致的恶性表型增强。总之,我们的研究结果表明,KIAA1429和CA9是OSCC中的促癌因子,其中KIAA1429通过m6A修饰依赖性稳定CA9转录物来促进OSCC的恶性发展,这代表了OSCC中一种新的调控机制。
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 求助全文
来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信