{"title":"Potential mechanism of circKIAA1429 accelerating the progression of hepatocellular carcinoma.","authors":"Yiting Yuan, Junwei Huang, Guifen Wei, Guang Hu, Hongmei Yu, Yiming Tao","doi":"10.1186/s13027-025-00645-3","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>This study investigates the underlying mechanism of circKIAA1429 (hsa_circ_0084922) in hepatocellular carcinoma (HCC) progression.</p><p><strong>Methods: </strong>circKIAA1429, SETD1A, NAP1L3, and GLIS2 expressions in HCC cells were detected by RT-qPCR or western blot. The stability of circKIAA1429 was tested after treatment with actinomycin D and Rnase R enzyme. circKIAA1429 expression was knocked down, followed by detection of cell proliferation, apoptosis, and migration/invasion using CCK-8, flow cytometry, and transwell. RIP and RNA pull-down were performed to validate the binding between circKIAA1429 and SETD1A, while ChIP analysis determined the enrichment of SETD1A and H3K4me3 or H3K27me3 on GLIS2 or NAP1L3 promoter. A nude mouse xenograft tumor model was establish to test the effect of circKIAA1429 on tumorigenicity.</p><p><strong>Results: </strong>circKIAA1429 and NAP1L3 were highly expressed in HCC cells, while GLIS2 was poorly expressed. Knockdown of circKIAA1429 repressed cell proliferation/invasion/migration and facilitated apoptosis. Mechanistically, circKIAA1429 directly interacted with SETD1A to reduce the enrichment of SETD1A and H3K4me3 or H3K27me3 on GLIS2 or NAP1L3 promoter, thus diminishing GLIS2 expression and elevating NAP1L3 expression. In vivo, circKIAA1429 promotes tumorigenesis via GLIS2/NAP1L3.</p><p><strong>Conclusion: </strong>circKIAA1429 interacts with SETD1A to inhibit the enrichment of H3K4me3 and H3K27me3 on GLIS2 or NAP1L3 promoter, thus inhibiting/promoting the expression of GLIS2/NAP1L3 and accelerating the progression of HCC.</p>","PeriodicalId":13568,"journal":{"name":"Infectious Agents and Cancer","volume":"20 1","pages":"12"},"PeriodicalIF":3.1000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11872318/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infectious Agents and Cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13027-025-00645-3","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: This study investigates the underlying mechanism of circKIAA1429 (hsa_circ_0084922) in hepatocellular carcinoma (HCC) progression.
Methods: circKIAA1429, SETD1A, NAP1L3, and GLIS2 expressions in HCC cells were detected by RT-qPCR or western blot. The stability of circKIAA1429 was tested after treatment with actinomycin D and Rnase R enzyme. circKIAA1429 expression was knocked down, followed by detection of cell proliferation, apoptosis, and migration/invasion using CCK-8, flow cytometry, and transwell. RIP and RNA pull-down were performed to validate the binding between circKIAA1429 and SETD1A, while ChIP analysis determined the enrichment of SETD1A and H3K4me3 or H3K27me3 on GLIS2 or NAP1L3 promoter. A nude mouse xenograft tumor model was establish to test the effect of circKIAA1429 on tumorigenicity.
Results: circKIAA1429 and NAP1L3 were highly expressed in HCC cells, while GLIS2 was poorly expressed. Knockdown of circKIAA1429 repressed cell proliferation/invasion/migration and facilitated apoptosis. Mechanistically, circKIAA1429 directly interacted with SETD1A to reduce the enrichment of SETD1A and H3K4me3 or H3K27me3 on GLIS2 or NAP1L3 promoter, thus diminishing GLIS2 expression and elevating NAP1L3 expression. In vivo, circKIAA1429 promotes tumorigenesis via GLIS2/NAP1L3.
Conclusion: circKIAA1429 interacts with SETD1A to inhibit the enrichment of H3K4me3 and H3K27me3 on GLIS2 or NAP1L3 promoter, thus inhibiting/promoting the expression of GLIS2/NAP1L3 and accelerating the progression of HCC.
期刊介绍：
Infectious Agents and Cancer is an open access, peer-reviewed online journal that encompasses all aspects of basic, clinical, epidemiological and translational research providing an insight into the association between chronic infections and cancer.
The journal welcomes submissions in the pathogen-related cancer areas and other related topics, in particular:
• HPV and anogenital cancers, as well as head and neck cancers;
• EBV and Burkitt lymphoma;
• HCV/HBV and hepatocellular carcinoma as well as lymphoproliferative diseases;
• HHV8 and Kaposi sarcoma;
• HTLV and leukemia;
• Cancers in Low- and Middle-income countries.
The link between infection and cancer has become well established over the past 50 years, and infection-associated cancer contribute up to 16% of cancers in developed countries and 33% in less developed countries.
Preventive vaccines have been developed for only two cancer-causing viruses, highlighting both the opportunity to prevent infection-associated cancers by vaccination and the gaps that remain before vaccines can be developed for other cancer-causing agents. These gaps are due to incomplete understanding of the basic biology, natural history, epidemiology of many of the pathogens that cause cancer, the mechanisms they exploit to cause cancer, and how to interrupt progression to cancer in human populations. Early diagnosis or identification of lesions at high risk of progression represent the current most critical research area of the field supported by recent advances in genomics and proteomics technologies.
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
