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DDB1- and CUL4-associated factor 13 (DCAF13), a substrate-recognition component of CRL4 E3 ubiquitin ligase, has an unclear mechanism in this disease. This study shows DCAF13 is highly expressed in human ovarian cancer, correlates inversely with overall survival, and suppresses proliferation, colony formation, and migration after CRISPR/Cas9 knockout, with reduced tumor growth in nude mice. Mechanistically, CRL4-DCAF13 targets FRAS1 for ubiquitination and degradation, activating FAK signaling and promoting tumorigenesis.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/dcaf13-promotes-ovarian-cancer-progression-by-activating-fras1-mediated-fak-signaling-pathway-abstract-and-results/332578/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/dcaf13-promotes-ovarian-cancer-progression-by-activating-fras1-mediated-fak-signaling-pathway-abstract-and-results/332578.png","ImageObject",300,407,{"name":92,"@type":93},"Riley","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-26","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":29},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What is DCAF13’s relationship to ovarian cancer outcomes?","Question",{"text":112,"@type":113},"DCAF13 is highly expressed in human ovarian cancer and its expression is negatively correlated with patients’ overall survival rate.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does DCAF13 knockout affect ovarian cancer cells?",{"text":117,"@type":113},"CRISPR/Cas9 knockout of DCAF13 significantly inhibits proliferation, colony formation, and migration of human ovarian cancer cells, and reduces tumor proliferation in nude mice.",{"name":119,"@type":110,"acceptedAnswer":120},"What molecular mechanism links DCAF13 to tumor progression?",{"text":121,"@type":113},"CRL4-DCAF13 mediates polyubiquitination and proteasomal degradation of FRAS1, and FRAS1 then influences proliferation and migration through induction of the focal adhesion kinase (FAK) signaling pathway.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},332578,1790534834,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":29,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145,"preview_page_count":4},1374391975076,"https://ap-avatar.wpscdn.com/avatar/14000253ca4ec9f6853?x-image-process=image/resize,m_fixed,w_180,h_180&k=1783305029341752051","Cellular and Molecular Life Sciences (2024) 81:421  \n[https://doi.org/10.1007/s00018-024-05446-2](https://doi.org/10.1007/s00018-024-05446-2) Cellular and Molecular Life Sciences  \nORIGINAL ARTICLE  \nDCAF13 promotes ovarian cancer progression by activating FRAS1-mediated FAK signaling pathway  \nZe-Yi Tang1,2,15 · Xiao-Min Wang1 · Chun-Wei Xu3 · Qing-Qing Sun1,2 · Yu-Xin Hua1,4 · Qi-Yin Zhou1,4 · Han-Yin Hu1,4 · Sheng-Bing Liu1 · Yan-Jun Guo1 · Lei Ao1 · Xuan Che5 · Xian-Chao Zhang6 · Michal Heger7,8,9 · Xin Zheng10 ·  \nAi-Jun Liu11 · Qian Wang12 · Zha-Jun Zhan2 · Shu-Qun Cheng1,13 · Wei-Wei Pan1,14  \nReceived: 21 April 2024 / Revised: 9 August 2024 / Accepted: 10 September 2024 © The Author(s) 2024  \nAbstract  \nCullin-RING ubiquitin ligase 4 (CRL4) is closely correlated with the incidence and progression of ovarian cancer. DDB1-and CUL4-associated factor 13 (DCAF13), a substrate-recognition protein in the CRL4 E3 ubiquitin ligase complex, is involved in the occurrence and development of ovarian cancer. However, its precise function and the underlying molecular mechanism in this disease remain unclear. In this study, we confirmed that DCAF13 is highly expressed in human ovarian cancer and its expression is negatively correlated with the overall survival rate of patients with ovarian cancer. We then used CRISPR/Cas9 to knockout DCAF13 and found that its deletion significantly inhibited the proliferation, colony formation, and migration of human ovarian cancer cells. In addition, DCAF13 deficiency inhibited tumor proliferation in nude mice. Mechanistically, CRL4-DCAF13 targeted Fraser extracellular matrix complex subunit 1 (FRAS1) for polyubiquitination and proteasomal degradation. FRAS1 influenced the proliferation and migration of ovarian cancer cell through induction of the focal adhesion kinase (FAK) signaling pathway. These findings collectively show that DCAF13 is an important oncogene that promotes tumorigenesis in ovarian cancer cells by mediating FRAS1/FAK signaling. Our findings provide a foundation for the development of targeted therapeutics for ovarian cancer.  \nKeywords Ovarian cancer · DCAF13 · FRAS1 · CRL4 E3 ubiquitin ligase · FAK  \nIntroduction  \nOvarian cancer is a common malignant tumor of the female reproductive system and has a high mortality rate among gynecological cancers [1] . Ovarian cancer typically proceeds undetected and lacks specific clinical symptoms in early stages [2] . Accordingly, more than 70% of patients with ovarian cancer are diagnosed in late stages, which are associated with extensive metastasis and poor prognosis [3] . Currently, surgical resection combined with chemotherapy is the standard treatment for ovarian cancer. However, the 5-year survival rate of patients with advanced disease remains less than 40%[4] . With prolonged chemotherapy cycles and multiple relapses, the sensitivity of most ovarian cancers to chemotherapeutic drugs gradually decreases,  \nZe-Yi Tang, Xiao-Min Wang and Chun-Wei Xu contributed equally to this work.  \nExtended author information available on the last page of the article  \nultimately leading to therapeutic recalcitrance [5] . Therefore, studies are urgently needed to understand the pathogenesis of ovarian cancer to improve prognosis and reduce mortality.  \nCullin-RING ubiquitin ligase 4 (CRL4) is an important member of the E3 ubiquitin ligase family. The CRL4 E3 ubiquitin ligase consists of three components, the scaffold protein CUL4, RING finger protein RBX1 (also known as ROC1 or HRT1), and DNA damage binding protein 1 (DDB1) [6] . Numerous studies showed that the CRL4 complex plays an important role in ovarian cancer [7–9] . DDB1-and CUL4-associated factor 13 (DCAF13), a substrate recognition protein for the CRL4 E3 ubiquitin ligase complex, is highly amplified in breast, liver, and lung cancer [10–14]. An early discovery by our group suggested that  \n1 3  \nDCAF13 is involved in cell cycle regulation, apoptosis, tumor-related signaling pathways, and ot","cbCaicHyTcehy8js","https://ap.wps.com/l/cbCaicHyTcehy8js","pdf",12557406,18,"English","# Abstract\n## DCAF13 expression and patient prognosis\n## Functional effects of DCAF13 knockout\n## Mechanism: CRL4-DCAF13 targets FRAS1 and activates FAK","[{\"question\":\"What is DCAF13’s relationship to ovarian cancer outcomes?\",\"answer\":\"DCAF13 is highly expressed in human ovarian cancer and its expression is negatively correlated with patients’ overall survival rate.\"},{\"question\":\"How does DCAF13 knockout affect ovarian cancer cells?\",\"answer\":\"CRISPR/Cas9 knockout of DCAF13 significantly inhibits proliferation, colony formation, and migration of human ovarian cancer cells, and reduces tumor proliferation in nude mice.\"},{\"question\":\"What molecular mechanism links DCAF13 to tumor progression?\",\"answer\":\"CRL4-DCAF13 mediates polyubiquitination and proteasomal degradation of FRAS1, and FRAS1 then influences proliferation and migration through induction of the focal adhesion kinase (FAK) signaling pathway.\"}]","DCAF13 promotes ovarian cancer progression by activating FRAS1-mediated FAK signaling pathway - Abstract and results | PDF",1789998795,45]