{"title":"FCH结构域仅1 (FCHO1)在肺癌中的致癌基因作用","authors":"M. Cho, S. Park, Soon‐Kyung Hwang","doi":"10.33696/signaling.3.070","DOIUrl":null,"url":null,"abstract":"Akt, or protein kinase B, a serine/threonine protein kinase [4], is activated downstream from phosphatidylinositol 3-kinase (PI3K), by various growth factors, including insulin, insulin-like growth factor-I, and epidermal growth factor [5]. Activated Akt (phospho-Akt, p-Akt) is a strong promoter of cell survival because it antagonizes and inactivates various components of the apoptotic cascade such as proapoptotic Bad, caspase-9, and forkhead transcription factor family members [6,7]. The PI3K/Akt signaling pathway regulates the G1/S cell cycle transition by modulating the transcription of cell cycle proteins and suppressing cell cycle inhibitors [8]. A dysregulated cell cycle is often associated with increased tumorigenesis and accelerated tumor growth [9].","PeriodicalId":73645,"journal":{"name":"Journal of cellular signaling","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Role of FCH Domain Only 1 (FCHO1) as an Oncogene in Lung Cancer\",\"authors\":\"M. Cho, S. Park, Soon‐Kyung Hwang\",\"doi\":\"10.33696/signaling.3.070\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Akt, or protein kinase B, a serine/threonine protein kinase [4], is activated downstream from phosphatidylinositol 3-kinase (PI3K), by various growth factors, including insulin, insulin-like growth factor-I, and epidermal growth factor [5]. Activated Akt (phospho-Akt, p-Akt) is a strong promoter of cell survival because it antagonizes and inactivates various components of the apoptotic cascade such as proapoptotic Bad, caspase-9, and forkhead transcription factor family members [6,7]. The PI3K/Akt signaling pathway regulates the G1/S cell cycle transition by modulating the transcription of cell cycle proteins and suppressing cell cycle inhibitors [8]. A dysregulated cell cycle is often associated with increased tumorigenesis and accelerated tumor growth [9].\",\"PeriodicalId\":73645,\"journal\":{\"name\":\"Journal of cellular signaling\",\"volume\":\"1 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-06-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of cellular signaling\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.33696/signaling.3.070\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of cellular signaling","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.33696/signaling.3.070","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The Role of FCH Domain Only 1 (FCHO1) as an Oncogene in Lung Cancer
Akt, or protein kinase B, a serine/threonine protein kinase [4], is activated downstream from phosphatidylinositol 3-kinase (PI3K), by various growth factors, including insulin, insulin-like growth factor-I, and epidermal growth factor [5]. Activated Akt (phospho-Akt, p-Akt) is a strong promoter of cell survival because it antagonizes and inactivates various components of the apoptotic cascade such as proapoptotic Bad, caspase-9, and forkhead transcription factor family members [6,7]. The PI3K/Akt signaling pathway regulates the G1/S cell cycle transition by modulating the transcription of cell cycle proteins and suppressing cell cycle inhibitors [8]. A dysregulated cell cycle is often associated with increased tumorigenesis and accelerated tumor growth [9].