Ying Zhou, Kailing Fan, Ning Dou, Li Li, Jialin Wang, Jingde Chen, Yandong Li, Yong Gao
{"title":"YTHDF2通过不依赖m6A修饰而上调PPP2CA在胃癌中发挥抑瘤作用。","authors":"Ying Zhou, Kailing Fan, Ning Dou, Li Li, Jialin Wang, Jingde Chen, Yandong Li, Yong Gao","doi":"10.1186/s12575-023-00195-1","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>YTHDF2 is one of important readers of N6-methyladenosine (m<sup>6</sup>A) modification on RNA. Growing evidence implicates that YTHDF2 takes an indispensable part in the regulation of tumorigenesis and metastasis in different cancers, but its biological functions and underlying mechanisms remain elusive in gastric cancer (GC).</p><p><strong>Aim: </strong>To investigate the clinical relevance and biological function of YTHDF2 in GC.</p><p><strong>Results: </strong>Compared with matched normal stomach tissues, YTHDF2 expression was markedly decreased in gastric cancer tissues. The expression level of YTHDF2 was inversely associated with gastric cancer patients' tumor size, AJCC classification and prognosis. Functionally, YTHDF2 reduction facilitated gastric cancer cell growth and migration in vitro and in vivo, whereas YTHDF2 overexpression exhibited opposite phenotypes. Mechanistically, YTHDF2 enhanced expression of PPP2CA, the catalytic subunit of PP2A (Protein phosphatase 2A), in an m<sup>6</sup>A-independent manner, and silencing of PPP2CA antagonized the anti-tumor effects caused by overexpression of YTHDF2 in GC cells.</p><p><strong>Conclusion: </strong>These findings demonstrate that YTHDF2 is down-regulated in GC and its down-regulation promotes GC progression via a possible mechanism involving PPP2CA expression, suggesting that YTHDF2 may be a hopeful biomarker for diagnosis and an unrevealed treatment target for GC.</p>","PeriodicalId":8960,"journal":{"name":"Biological Procedures Online","volume":"25 1","pages":"6"},"PeriodicalIF":3.7000,"publicationDate":"2023-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9985201/pdf/","citationCount":"1","resultStr":"{\"title\":\"YTHDF2 exerts tumor-suppressor roles in gastric cancer via up-regulating PPP2CA independently of m<sup>6</sup>A modification.\",\"authors\":\"Ying Zhou, Kailing Fan, Ning Dou, Li Li, Jialin Wang, Jingde Chen, Yandong Li, Yong Gao\",\"doi\":\"10.1186/s12575-023-00195-1\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>YTHDF2 is one of important readers of N6-methyladenosine (m<sup>6</sup>A) modification on RNA. Growing evidence implicates that YTHDF2 takes an indispensable part in the regulation of tumorigenesis and metastasis in different cancers, but its biological functions and underlying mechanisms remain elusive in gastric cancer (GC).</p><p><strong>Aim: </strong>To investigate the clinical relevance and biological function of YTHDF2 in GC.</p><p><strong>Results: </strong>Compared with matched normal stomach tissues, YTHDF2 expression was markedly decreased in gastric cancer tissues. The expression level of YTHDF2 was inversely associated with gastric cancer patients' tumor size, AJCC classification and prognosis. Functionally, YTHDF2 reduction facilitated gastric cancer cell growth and migration in vitro and in vivo, whereas YTHDF2 overexpression exhibited opposite phenotypes. Mechanistically, YTHDF2 enhanced expression of PPP2CA, the catalytic subunit of PP2A (Protein phosphatase 2A), in an m<sup>6</sup>A-independent manner, and silencing of PPP2CA antagonized the anti-tumor effects caused by overexpression of YTHDF2 in GC cells.</p><p><strong>Conclusion: </strong>These findings demonstrate that YTHDF2 is down-regulated in GC and its down-regulation promotes GC progression via a possible mechanism involving PPP2CA expression, suggesting that YTHDF2 may be a hopeful biomarker for diagnosis and an unrevealed treatment target for GC.</p>\",\"PeriodicalId\":8960,\"journal\":{\"name\":\"Biological Procedures Online\",\"volume\":\"25 1\",\"pages\":\"6\"},\"PeriodicalIF\":3.7000,\"publicationDate\":\"2023-03-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9985201/pdf/\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biological Procedures Online\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1186/s12575-023-00195-1\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMICAL RESEARCH METHODS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biological Procedures Online","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s12575-023-00195-1","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMICAL RESEARCH METHODS","Score":null,"Total":0}
YTHDF2 exerts tumor-suppressor roles in gastric cancer via up-regulating PPP2CA independently of m6A modification.
Background: YTHDF2 is one of important readers of N6-methyladenosine (m6A) modification on RNA. Growing evidence implicates that YTHDF2 takes an indispensable part in the regulation of tumorigenesis and metastasis in different cancers, but its biological functions and underlying mechanisms remain elusive in gastric cancer (GC).
Aim: To investigate the clinical relevance and biological function of YTHDF2 in GC.
Results: Compared with matched normal stomach tissues, YTHDF2 expression was markedly decreased in gastric cancer tissues. The expression level of YTHDF2 was inversely associated with gastric cancer patients' tumor size, AJCC classification and prognosis. Functionally, YTHDF2 reduction facilitated gastric cancer cell growth and migration in vitro and in vivo, whereas YTHDF2 overexpression exhibited opposite phenotypes. Mechanistically, YTHDF2 enhanced expression of PPP2CA, the catalytic subunit of PP2A (Protein phosphatase 2A), in an m6A-independent manner, and silencing of PPP2CA antagonized the anti-tumor effects caused by overexpression of YTHDF2 in GC cells.
Conclusion: These findings demonstrate that YTHDF2 is down-regulated in GC and its down-regulation promotes GC progression via a possible mechanism involving PPP2CA expression, suggesting that YTHDF2 may be a hopeful biomarker for diagnosis and an unrevealed treatment target for GC.
期刊介绍：
iological Procedures Online publishes articles that improve access to techniques and methods in the medical and biological sciences.
We are also interested in short but important research discoveries, such as new animal disease models.
Topics of interest include, but are not limited to:
Reports of new research techniques and applications of existing techniques
Technical analyses of research techniques and published reports
Validity analyses of research methods and approaches to judging the validity of research reports
Application of common research methods
Reviews of existing techniques
Novel/important product information
Biological Procedures Online places emphasis on multidisciplinary approaches that integrate methodologies from medicine, biology, chemistry, imaging, engineering, bioinformatics, computer science, and systems analysis.
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