Qian Du, Meiying Zhang, Aiai Gao, Tao He, Mingzhou Guo
{"title":"表观遗传沉默 ZSCAN23 通过激活 Wnt 信号促进胰腺癌生长","authors":"Qian Du, Meiying Zhang, Aiai Gao, Tao He, Mingzhou Guo","doi":"10.1080/15384047.2024.2302924","DOIUrl":null,"url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is the most malignant tumor. Zinc finger and SCAN domain-containing protein 23 (<i>ZSCAN23</i>) is a new member of the SCAN domain family. The expression regulation and biological function remain to be elucidated. In this study, we explored the epigenetic regulation and the function of <i>ZSCAN23</i> in PDAC. <i>ZSCAN23</i> was methylated in 60.21% (171/284) of PDAC and its expression was regulated by promoter region methylation. The expression of <i>ZSCAN23</i> inhibited cell proliferation, colony formation, migration, invasion, and induced apoptosis and G1/S phase arrest. <i>ZSCAN23</i> suppressed Panc10.05 cell xenograft growth in mice. Mechanistically, <i>ZSCAN23</i> inhibited Wnt signaling by interacting with myosin heavy chain 9 (MYH9) in pancreatic cancer cells. <i>ZSCAN23</i> is frequently methylated in PDAC and may serve as a detective marker. <i>ZSCAN23</i> suppresses PDAC cell growth both <i>in vitro</i> and <i>in vivo</i>.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"25 1","pages":"2302924"},"PeriodicalIF":4.4000,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10793710/pdf/","citationCount":"0","resultStr":"{\"title\":\"Epigenetic silencing <i>ZSCAN23</i> promotes pancreatic cancer growth by activating Wnt signaling.\",\"authors\":\"Qian Du, Meiying Zhang, Aiai Gao, Tao He, Mingzhou Guo\",\"doi\":\"10.1080/15384047.2024.2302924\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Pancreatic ductal adenocarcinoma (PDAC) is the most malignant tumor. Zinc finger and SCAN domain-containing protein 23 (<i>ZSCAN23</i>) is a new member of the SCAN domain family. The expression regulation and biological function remain to be elucidated. In this study, we explored the epigenetic regulation and the function of <i>ZSCAN23</i> in PDAC. <i>ZSCAN23</i> was methylated in 60.21% (171/284) of PDAC and its expression was regulated by promoter region methylation. The expression of <i>ZSCAN23</i> inhibited cell proliferation, colony formation, migration, invasion, and induced apoptosis and G1/S phase arrest. <i>ZSCAN23</i> suppressed Panc10.05 cell xenograft growth in mice. Mechanistically, <i>ZSCAN23</i> inhibited Wnt signaling by interacting with myosin heavy chain 9 (MYH9) in pancreatic cancer cells. <i>ZSCAN23</i> is frequently methylated in PDAC and may serve as a detective marker. <i>ZSCAN23</i> suppresses PDAC cell growth both <i>in vitro</i> and <i>in vivo</i>.</p>\",\"PeriodicalId\":9536,\"journal\":{\"name\":\"Cancer Biology & Therapy\",\"volume\":\"25 1\",\"pages\":\"2302924\"},\"PeriodicalIF\":4.4000,\"publicationDate\":\"2024-12-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10793710/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer Biology & Therapy\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/15384047.2024.2302924\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/16 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Biology & Therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15384047.2024.2302924","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/16 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
Epigenetic silencing ZSCAN23 promotes pancreatic cancer growth by activating Wnt signaling.
Pancreatic ductal adenocarcinoma (PDAC) is the most malignant tumor. Zinc finger and SCAN domain-containing protein 23 (ZSCAN23) is a new member of the SCAN domain family. The expression regulation and biological function remain to be elucidated. In this study, we explored the epigenetic regulation and the function of ZSCAN23 in PDAC. ZSCAN23 was methylated in 60.21% (171/284) of PDAC and its expression was regulated by promoter region methylation. The expression of ZSCAN23 inhibited cell proliferation, colony formation, migration, invasion, and induced apoptosis and G1/S phase arrest. ZSCAN23 suppressed Panc10.05 cell xenograft growth in mice. Mechanistically, ZSCAN23 inhibited Wnt signaling by interacting with myosin heavy chain 9 (MYH9) in pancreatic cancer cells. ZSCAN23 is frequently methylated in PDAC and may serve as a detective marker. ZSCAN23 suppresses PDAC cell growth both in vitro and in vivo.
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Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
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