Tianhao Wu, Zhongxiang Xiao, Bowen Su, Zaihua Yan, Yv Zhao, Cheng Huang, Lu Zhou, Hongpeng Tian, Guangjun Zhang
{"title":"剪接因子3b亚基4 （SF3b4）由EP300和CREBBP介导，通过增强自噬促进结直肠癌（CRC）的增殖。","authors":"Tianhao Wu, Zhongxiang Xiao, Bowen Su, Zaihua Yan, Yv Zhao, Cheng Huang, Lu Zhou, Hongpeng Tian, Guangjun Zhang","doi":"10.62347/AHXI2343","DOIUrl":null,"url":null,"abstract":"<p><p>Splicing factor 3b subunit 4 (SF3b4) is closely associated with cancer development. As a core subunit of the SF3b complex, SF3b4 participates in regulating alternative splicing, and its abnormal expression is linked to the onset of malignant tumors. However, the role of SF3b4 in colorectal cancer (CRC) remains undefined. This study demonstrates that in CRC, E1A binding protein p300 (EP300) and CREB binding protein (CREBBP) regulate SF3b4 expression by activating Histone H3 lysine 27 acetylation (H3K27ac) on the SF3b4 promoter. Additionally, enhanced autophagy counteracts the proliferation-inhibitory effect of SF3b4 knockdown in CRC cells. Implications Statement: SF3b4 may promote CRC proliferation by enhancing cellular autophagy. SF3b4 acts as a potential oncogene in CRC tumorigenesis and progression. SF3b4 serves as a promising prognostic biomarker for CRC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"15 6","pages":"2826-2842"},"PeriodicalIF":2.9000,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256420/pdf/","citationCount":"0","resultStr":"{\"title\":\"Splicing factor 3b subunit 4 (SF3b4) is mediated by EP300 and CREBBP to promote colorectal cancer (CRC) proliferation by enhancing autophagy.\",\"authors\":\"Tianhao Wu, Zhongxiang Xiao, Bowen Su, Zaihua Yan, Yv Zhao, Cheng Huang, Lu Zhou, Hongpeng Tian, Guangjun Zhang\",\"doi\":\"10.62347/AHXI2343\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Splicing factor 3b subunit 4 (SF3b4) is closely associated with cancer development. As a core subunit of the SF3b complex, SF3b4 participates in regulating alternative splicing, and its abnormal expression is linked to the onset of malignant tumors. However, the role of SF3b4 in colorectal cancer (CRC) remains undefined. This study demonstrates that in CRC, E1A binding protein p300 (EP300) and CREB binding protein (CREBBP) regulate SF3b4 expression by activating Histone H3 lysine 27 acetylation (H3K27ac) on the SF3b4 promoter. Additionally, enhanced autophagy counteracts the proliferation-inhibitory effect of SF3b4 knockdown in CRC cells. Implications Statement: SF3b4 may promote CRC proliferation by enhancing cellular autophagy. SF3b4 acts as a potential oncogene in CRC tumorigenesis and progression. SF3b4 serves as a promising prognostic biomarker for CRC.</p>\",\"PeriodicalId\":7437,\"journal\":{\"name\":\"American journal of cancer research\",\"volume\":\"15 6\",\"pages\":\"2826-2842\"},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2025-06-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12256420/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of cancer research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.62347/AHXI2343\",\"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/AHXI2343","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}
Splicing factor 3b subunit 4 (SF3b4) is mediated by EP300 and CREBBP to promote colorectal cancer (CRC) proliferation by enhancing autophagy.
Splicing factor 3b subunit 4 (SF3b4) is closely associated with cancer development. As a core subunit of the SF3b complex, SF3b4 participates in regulating alternative splicing, and its abnormal expression is linked to the onset of malignant tumors. However, the role of SF3b4 in colorectal cancer (CRC) remains undefined. This study demonstrates that in CRC, E1A binding protein p300 (EP300) and CREB binding protein (CREBBP) regulate SF3b4 expression by activating Histone H3 lysine 27 acetylation (H3K27ac) on the SF3b4 promoter. Additionally, enhanced autophagy counteracts the proliferation-inhibitory effect of SF3b4 knockdown in CRC cells. Implications Statement: SF3b4 may promote CRC proliferation by enhancing cellular autophagy. SF3b4 acts as a potential oncogene in CRC tumorigenesis and progression. SF3b4 serves as a promising prognostic biomarker for CRC.
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.
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