KM04416 suppressed lung adenocarcinoma progression by promoting immune infiltration.

IF 1.5 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Yalan Lin, Weijing Wu, Huihuang Lin, Shiyuan Chen, Huiying Lv, Shuchao Chen, Chuzhao Li, Xinwen Wang, Yunfeng Chen
{"title":"KM04416 suppressed lung adenocarcinoma progression by promoting immune infiltration.","authors":"Yalan Lin, Weijing Wu, Huihuang Lin, Shiyuan Chen, Huiying Lv, Shuchao Chen, Chuzhao Li, Xinwen Wang, Yunfeng Chen","doi":"10.1186/s13019-024-02971-w","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>Lung adenocarcinoma (LUAD) is a malignant tumor originating from the bronchial mucosa or glands of the lung, with the fastest increasing morbidity and mortality. Therefore, the prognosis of lung cancer remains poor. Glycerol-3-phosphate dehydrogenase 2 (GPD2) is a widely existing protein pattern sequence in biology and is closely related to tumor progression. The therapy values of GPD2 inhibitor in LUAD were unclear. Therefore, we aimed to analyze the therapy values of GPD2 inhibitor in LUAD.</p><p><strong>Materials and methods: </strong>The Cancer Genome Atlas (TCGA)-LUAD database was used to analyze the expression levels of GPD2 in LUAD tissues. The relationship between GPD2 expression and LUAD patient survival was analyzed by Kaplan-Meier method. Moreover, KM04416 as a target inhibitor of GPD2 was used to further investigate the therapy value of GPD2 inhibitor in LUAD cells lines (A549 cell and H1299 cell). The TISIDB website was used to investigate the associations between GPD2 expression and immune cell infiltration in LUAD.</p><p><strong>Results: </strong>The results showed that GPD2 is overexpressed in LUAD tissues and significantly associated with poor survival. KM04416 can suppress the progression of LUAD cells by targeting GPD2. Low expression of GPD2 is related to high infiltration of immune cells.</p><p><strong>Conclusions: </strong>In summary, our present study found that targeting inhibition of GPD2 by KM04416 can suppress LUAD progression via adjusting immune cell infiltration.</p>","PeriodicalId":15201,"journal":{"name":"Journal of Cardiothoracic Surgery","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11270931/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cardiothoracic Surgery","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13019-024-02971-w","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0

Abstract

Objectives: Lung adenocarcinoma (LUAD) is a malignant tumor originating from the bronchial mucosa or glands of the lung, with the fastest increasing morbidity and mortality. Therefore, the prognosis of lung cancer remains poor. Glycerol-3-phosphate dehydrogenase 2 (GPD2) is a widely existing protein pattern sequence in biology and is closely related to tumor progression. The therapy values of GPD2 inhibitor in LUAD were unclear. Therefore, we aimed to analyze the therapy values of GPD2 inhibitor in LUAD.

Materials and methods: The Cancer Genome Atlas (TCGA)-LUAD database was used to analyze the expression levels of GPD2 in LUAD tissues. The relationship between GPD2 expression and LUAD patient survival was analyzed by Kaplan-Meier method. Moreover, KM04416 as a target inhibitor of GPD2 was used to further investigate the therapy value of GPD2 inhibitor in LUAD cells lines (A549 cell and H1299 cell). The TISIDB website was used to investigate the associations between GPD2 expression and immune cell infiltration in LUAD.

Results: The results showed that GPD2 is overexpressed in LUAD tissues and significantly associated with poor survival. KM04416 can suppress the progression of LUAD cells by targeting GPD2. Low expression of GPD2 is related to high infiltration of immune cells.

Conclusions: In summary, our present study found that targeting inhibition of GPD2 by KM04416 can suppress LUAD progression via adjusting immune cell infiltration.

KM04416 可通过促进免疫浸润来抑制肺腺癌的进展。
研究目的肺腺癌(LUAD)是一种起源于肺部支气管粘膜或腺体的恶性肿瘤,发病率和死亡率增长最快。因此,肺癌的预后仍然很差。甘油-3-磷酸脱氢酶 2(GPD2)是生物学中广泛存在的一种蛋白模式序列,与肿瘤进展密切相关。GPD2抑制剂在LUAD中的治疗价值尚不明确。因此,我们旨在分析GPD2抑制剂在LUAD中的治疗价值:采用癌症基因组图谱(TCGA)-LUAD数据库分析GPD2在LUAD组织中的表达水平。采用Kaplan-Meier方法分析了GPD2表达与LUAD患者生存率之间的关系。此外,以KM04416作为GPD2的靶向抑制剂,进一步研究了GPD2抑制剂在LUAD细胞系(A549细胞和H1299细胞)中的治疗价值。利用TISIDB网站研究了LUAD中GPD2表达与免疫细胞浸润之间的关联:结果:研究结果表明,GPD2在LUAD组织中过表达,并与不良生存率显著相关。KM04416可通过靶向GPD2抑制LUAD细胞的进展。GPD2的低表达与免疫细胞的高浸润有关:综上所述,本研究发现,KM04416靶向抑制GPD2可通过调整免疫细胞浸润来抑制LUAD的进展。
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
Journal of Cardiothoracic Surgery
Journal of Cardiothoracic Surgery 医学-心血管系统
CiteScore
2.50
自引率
6.20%
发文量
286
审稿时长
4-8 weeks
期刊介绍: Journal of Cardiothoracic Surgery is an open access journal that encompasses all aspects of research in the field of Cardiology, and Cardiothoracic and Vascular Surgery. The journal publishes original scientific research documenting clinical and experimental advances in cardiac, vascular and thoracic surgery, and related fields. Topics of interest include surgical techniques, survival rates, surgical complications and their outcomes; along with basic sciences, pediatric conditions, transplantations and clinical trials. Journal of Cardiothoracic Surgery is of interest to cardiothoracic and vascular surgeons, cardiothoracic anaesthesiologists, cardiologists, chest physicians, and allied health professionals.
文献相关原料
公司名称 产品信息 采购帮参考价格
×
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