{"title":"SCARA5可能是CC的一个潜在标记物，并促进FTL引起的铁下垂。","authors":"Wenjing Qi, Shunan Zhang","doi":"10.62347/CGEJ9093","DOIUrl":null,"url":null,"abstract":"<p><p>The current investigation sought to explore the effects and its possible mechanisms of Scavenger receptor class A member 5 (SCARA5) in model of colon cancer (CC). Patients diagnosed with CC were recruited from our hospital. SCARA5 mRNA expression levels in patients with CC was reduced, and the expression of SCARA5 mRNA in patients with I-II was higher than that of patients with III-IV. The overall survival (OS) and disease-free survival (DFS) of SCARA5 high expression were higher those of SCARA5 low expression in patients with CC. Sh-SCARA5 promoted CC in mice model. SCARA5 up-regulation reduced cell growth of CC. SCARA5 up-regulation promoted Ferroptosis of CC by the inhibition of mitochondrial damage. SCARA5 up-regulation induced ferritin light chain (FTL) protein expression. Si-FTL attenuated the effects of SCARA5 on Ferroptosis in CC. The SCARA5 protein interlinked with the FTL protein. SCARA5 up-regulation reduced FTL protein ubiquitination. Up-regulation of SCARA5 suppressed cell growth in CC. SCARA5 up-regulation enhanced ferroptosis in CC by inhibiting mitochondrial damage. We conclude that SCARA5 promoted ferroptosis in CC cells by inhibiting FTL ubiquitination-induced mitochondrial damage, which may contribute to the treatment of CC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 2","pages":"426-438"},"PeriodicalIF":3.6000,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897624/pdf/","citationCount":"0","resultStr":"{\"title\":\"SCARA5 might be one potential marker for CC and promoted Ferroptosis by FTL.\",\"authors\":\"Wenjing Qi, Shunan Zhang\",\"doi\":\"10.62347/CGEJ9093\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The current investigation sought to explore the effects and its possible mechanisms of Scavenger receptor class A member 5 (SCARA5) in model of colon cancer (CC). Patients diagnosed with CC were recruited from our hospital. SCARA5 mRNA expression levels in patients with CC was reduced, and the expression of SCARA5 mRNA in patients with I-II was higher than that of patients with III-IV. The overall survival (OS) and disease-free survival (DFS) of SCARA5 high expression were higher those of SCARA5 low expression in patients with CC. Sh-SCARA5 promoted CC in mice model. SCARA5 up-regulation reduced cell growth of CC. SCARA5 up-regulation promoted Ferroptosis of CC by the inhibition of mitochondrial damage. SCARA5 up-regulation induced ferritin light chain (FTL) protein expression. Si-FTL attenuated the effects of SCARA5 on Ferroptosis in CC. The SCARA5 protein interlinked with the FTL protein. SCARA5 up-regulation reduced FTL protein ubiquitination. Up-regulation of SCARA5 suppressed cell growth in CC. SCARA5 up-regulation enhanced ferroptosis in CC by inhibiting mitochondrial damage. We conclude that SCARA5 promoted ferroptosis in CC cells by inhibiting FTL ubiquitination-induced mitochondrial damage, which may contribute to the treatment of CC.</p>\",\"PeriodicalId\":7437,\"journal\":{\"name\":\"American journal of cancer research\",\"volume\":\"15 2\",\"pages\":\"426-438\"},\"PeriodicalIF\":3.6000,\"publicationDate\":\"2025-02-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11897624/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of cancer research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.62347/CGEJ9093\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/CGEJ9093","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
SCARA5 might be one potential marker for CC and promoted Ferroptosis by FTL.
The current investigation sought to explore the effects and its possible mechanisms of Scavenger receptor class A member 5 (SCARA5) in model of colon cancer (CC). Patients diagnosed with CC were recruited from our hospital. SCARA5 mRNA expression levels in patients with CC was reduced, and the expression of SCARA5 mRNA in patients with I-II was higher than that of patients with III-IV. The overall survival (OS) and disease-free survival (DFS) of SCARA5 high expression were higher those of SCARA5 low expression in patients with CC. Sh-SCARA5 promoted CC in mice model. SCARA5 up-regulation reduced cell growth of CC. SCARA5 up-regulation promoted Ferroptosis of CC by the inhibition of mitochondrial damage. SCARA5 up-regulation induced ferritin light chain (FTL) protein expression. Si-FTL attenuated the effects of SCARA5 on Ferroptosis in CC. The SCARA5 protein interlinked with the FTL protein. SCARA5 up-regulation reduced FTL protein ubiquitination. Up-regulation of SCARA5 suppressed cell growth in CC. SCARA5 up-regulation enhanced ferroptosis in CC by inhibiting mitochondrial damage. We conclude that SCARA5 promoted ferroptosis in CC cells by inhibiting FTL ubiquitination-induced mitochondrial damage, which may contribute to the treatment of CC.
期刊介绍：
The American Journal of Cancer Research (AJCR) (ISSN 2156-6976), is an independent open access, online only journal to facilitate rapid dissemination of novel discoveries in basic science and treatment of cancer. It was founded by a group of scientists for cancer research and clinical academic oncologists from around the world, who are devoted to the promotion and advancement of our understanding of the cancer and its treatment. The scope of AJCR is intended to encompass that of multi-disciplinary researchers from any scientific discipline where the primary focus of the research is to increase and integrate knowledge about etiology and molecular mechanisms of carcinogenesis with the ultimate aim of advancing the cure and prevention of this increasingly devastating disease. To achieve these aims AJCR will publish review articles, original articles and new techniques in cancer research and therapy. It will also publish hypothesis, case reports and letter to the editor. Unlike most other open access online journals, AJCR will keep most of the traditional features of paper print that we are all familiar with, such as continuous volume, issue numbers, as well as continuous page numbers to retain our comfortable familiarity towards an academic journal.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
