METTL3 affects the biological function of lung adenocarcinoma through the FGF2/PI3K/AKT /mTOR pathway.

IF 3.5 3区 医学 Q2 ONCOLOGY Frontiers in Oncology Pub Date : 2024-10-21 eCollection Date: 2024-01-01 DOI:10.3389/fonc.2024.1474701
Shaoting Chen, Xiuqing Shen, Pengju Cao, Qianshun Chen, Rongxin Zhong, Yingping Cao
{"title":"METTL3 affects the biological function of lung adenocarcinoma through the FGF2/PI3K/AKT /mTOR pathway.","authors":"Shaoting Chen, Xiuqing Shen, Pengju Cao, Qianshun Chen, Rongxin Zhong, Yingping Cao","doi":"10.3389/fonc.2024.1474701","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>This study aims to investigate the role of the m6A regulatory factor METTL3 in LUAD.</p><p><strong>Methods: </strong>By examining the expression of METTL3 in LUAD and conducting cellular functional experiments, the biological functions of METTL3 were discussed. mRNA-seq and MeRIP-qPCR were used to identify downstream target genes and pathways.</p><p><strong>Results: </strong>The expression level of METTL3 in LUAD is lower than that in the control group. The downregulation of METTL3 promoted the proliferation, migration, and invasion of LUAD cells, while overexpression of METTL3 results in the opposite effects. Furthermore, we found that FGF2 was negatively regulated by METTL3. Inhibiting FGF2 reversed the tumor-promoting effects caused by METTL3 downregulation in LUAD cells. Silencing METTL3 enhanced the stability of FGF2 mRNA. Silencing FGF2 resulted in reduced activity of the PI3K/AKT/mTOR signaling pathway in METTL3 knockdown LUAD cells.</p><p><strong>Discussion: </strong>In summary, our findings unveil an intricate signaling network involving METTL3/FGF2/PI3K/AKT/mTOR in LUAD and provide valuable insights into the molecular mechanisms underlying tumor progression, thus holding significant implications for targeted therapy and advancing LUAD research.</p>","PeriodicalId":12482,"journal":{"name":"Frontiers in Oncology","volume":null,"pages":null},"PeriodicalIF":3.5000,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532124/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fonc.2024.1474701","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction: This study aims to investigate the role of the m6A regulatory factor METTL3 in LUAD.

Methods: By examining the expression of METTL3 in LUAD and conducting cellular functional experiments, the biological functions of METTL3 were discussed. mRNA-seq and MeRIP-qPCR were used to identify downstream target genes and pathways.

Results: The expression level of METTL3 in LUAD is lower than that in the control group. The downregulation of METTL3 promoted the proliferation, migration, and invasion of LUAD cells, while overexpression of METTL3 results in the opposite effects. Furthermore, we found that FGF2 was negatively regulated by METTL3. Inhibiting FGF2 reversed the tumor-promoting effects caused by METTL3 downregulation in LUAD cells. Silencing METTL3 enhanced the stability of FGF2 mRNA. Silencing FGF2 resulted in reduced activity of the PI3K/AKT/mTOR signaling pathway in METTL3 knockdown LUAD cells.

Discussion: In summary, our findings unveil an intricate signaling network involving METTL3/FGF2/PI3K/AKT/mTOR in LUAD and provide valuable insights into the molecular mechanisms underlying tumor progression, thus holding significant implications for targeted therapy and advancing LUAD research.

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
METTL3 通过 FGF2/PI3K/AKT /mTOR 通路影响肺腺癌的生物学功能。
简介:本研究旨在探讨 m6A 调控因子 METTL3 在 LUAD 中的作用:本研究旨在探讨m6A调控因子METTL3在LUAD中的作用:mRNA-seq和MeRIP-qPCR用于鉴定下游靶基因和通路:结果:METTL3在LUAD中的表达水平低于对照组。下调 METTL3 可促进 LUAD 细胞的增殖、迁移和侵袭,而过表达 METTL3 则会产生相反的效果。此外,我们还发现 FGF2 受 METTL3 的负调控。抑制 FGF2 可以逆转 METTL3 下调对 LUAD 细胞的肿瘤促进作用。沉默 METTL3 可增强 FGF2 mRNA 的稳定性。在METTL3敲除的LUAD细胞中,沉默FGF2可降低PI3K/AKT/mTOR信号通路的活性:总之,我们的研究结果揭示了LUAD中涉及METTL3/FGF2/PI3K/AKT/mTOR的复杂信号网络,为了解肿瘤进展的分子机制提供了有价值的见解,从而对靶向治疗和推进LUAD研究具有重要意义。
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
Frontiers in Oncology
Frontiers in Oncology Biochemistry, Genetics and Molecular Biology-Cancer Research
CiteScore
6.20
自引率
10.60%
发文量
6641
审稿时长
14 weeks
期刊介绍: Cancer Imaging and Diagnosis is dedicated to the publication of results from clinical and research studies applied to cancer diagnosis and treatment. The section aims to publish studies from the entire field of cancer imaging: results from routine use of clinical imaging in both radiology and nuclear medicine, results from clinical trials, experimental molecular imaging in humans and small animals, research on new contrast agents in CT, MRI, ultrasound, publication of new technical applications and processing algorithms to improve the standardization of quantitative imaging and image guided interventions for the diagnosis and treatment of cancer.
期刊最新文献
Clinical utility of circulating tumor DNA profiling in detecting targetable fusions in non-small cell lung cancer. Low miR-936-mediated upregulation of Pim-3 drives sorafenib resistance in liver cancer through ferroptosis inhibition by activating the ANKRD18A/Src/NRF2 pathway. Machine learning-based prediction of 5-year survival in elderly NSCLC patients using oxidative stress markers. Perirectal angioleiomyoma preoperatively misdiagnosed as rectal cancer: a case report. Prognostic value and immunomodulatory role of DNM1L in gastric adenocarcinoma.
×
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