{"title":"Forkhead Box S1通过介导Wnt/β-catenin通路抑制肺鳞癌细胞的进展。","authors":"Fei Wang, Song Li","doi":"10.4103/0304-4920.359799","DOIUrl":null,"url":null,"abstract":"<p><p>Lung squamous cell carcinoma (SCC) is considered the frequent subtype of non-small cell lung cancer (NSCLC) and results in high mortality worldwide every year. Forkhead box S1 (FOXS1) is correlated to multiple cancers, but the role and the mechanism of FOXS1 in lung SCC are unclear. This study revealed that FOXS1 was low expressed in the lung SCC tissues by utilizing UALCAN and TIMER databases. Western blotting analysis was introduced to estimate the FOXS1 expression in the lung SCC cells. Functionally, overexpression of FOXS1 dramatically inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition in the lung SCC cells. However, knockdown of FOXS1 exerted diverse effects on lung SCC cell progression. Moreover, FOXS1 overexpression suppressed tumor growth in nude mice remarkably. Furthermore, FOXS1 overexpression reduced the activity of Wnt/β-catenin signal, while FOXS1 silence reversed the roles notably. In conclusion, our present study proved that FOXS1 inhibited lung SCC development in vitro and in vivo might by modulating Wnt/β-catenin signaling pathway.</p>","PeriodicalId":1,"journal":{"name":"Accounts of Chemical Research","volume":null,"pages":null},"PeriodicalIF":16.4000,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Forkhead Box S1 inhibits the progression of lung squamous cell carcinoma cells by mediating Wnt/β-catenin pathway.\",\"authors\":\"Fei Wang, Song Li\",\"doi\":\"10.4103/0304-4920.359799\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Lung squamous cell carcinoma (SCC) is considered the frequent subtype of non-small cell lung cancer (NSCLC) and results in high mortality worldwide every year. Forkhead box S1 (FOXS1) is correlated to multiple cancers, but the role and the mechanism of FOXS1 in lung SCC are unclear. This study revealed that FOXS1 was low expressed in the lung SCC tissues by utilizing UALCAN and TIMER databases. Western blotting analysis was introduced to estimate the FOXS1 expression in the lung SCC cells. Functionally, overexpression of FOXS1 dramatically inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition in the lung SCC cells. However, knockdown of FOXS1 exerted diverse effects on lung SCC cell progression. Moreover, FOXS1 overexpression suppressed tumor growth in nude mice remarkably. Furthermore, FOXS1 overexpression reduced the activity of Wnt/β-catenin signal, while FOXS1 silence reversed the roles notably. In conclusion, our present study proved that FOXS1 inhibited lung SCC development in vitro and in vivo might by modulating Wnt/β-catenin signaling pathway.</p>\",\"PeriodicalId\":1,\"journal\":{\"name\":\"Accounts of Chemical Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":16.4000,\"publicationDate\":\"2022-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Accounts of Chemical Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.4103/0304-4920.359799\",\"RegionNum\":1,\"RegionCategory\":\"化学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CHEMISTRY, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Accounts of Chemical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.4103/0304-4920.359799","RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
Forkhead Box S1 inhibits the progression of lung squamous cell carcinoma cells by mediating Wnt/β-catenin pathway.
Lung squamous cell carcinoma (SCC) is considered the frequent subtype of non-small cell lung cancer (NSCLC) and results in high mortality worldwide every year. Forkhead box S1 (FOXS1) is correlated to multiple cancers, but the role and the mechanism of FOXS1 in lung SCC are unclear. This study revealed that FOXS1 was low expressed in the lung SCC tissues by utilizing UALCAN and TIMER databases. Western blotting analysis was introduced to estimate the FOXS1 expression in the lung SCC cells. Functionally, overexpression of FOXS1 dramatically inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition in the lung SCC cells. However, knockdown of FOXS1 exerted diverse effects on lung SCC cell progression. Moreover, FOXS1 overexpression suppressed tumor growth in nude mice remarkably. Furthermore, FOXS1 overexpression reduced the activity of Wnt/β-catenin signal, while FOXS1 silence reversed the roles notably. In conclusion, our present study proved that FOXS1 inhibited lung SCC development in vitro and in vivo might by modulating Wnt/β-catenin signaling pathway.
期刊介绍:
Accounts of Chemical Research presents short, concise and critical articles offering easy-to-read overviews of basic research and applications in all areas of chemistry and biochemistry. These short reviews focus on research from the author’s own laboratory and are designed to teach the reader about a research project. In addition, Accounts of Chemical Research publishes commentaries that give an informed opinion on a current research problem. Special Issues online are devoted to a single topic of unusual activity and significance.
Accounts of Chemical Research replaces the traditional article abstract with an article "Conspectus." These entries synopsize the research affording the reader a closer look at the content and significance of an article. Through this provision of a more detailed description of the article contents, the Conspectus enhances the article's discoverability by search engines and the exposure for the research.