{"title":"PRIM2 promotes proliferation and metastasis of pancreatic ductal adenocarcinoma through interactions with FAM111B.","authors":"Jingyang Yin, Fanbo Qin, Hui Chen, Xianxing Wang, Renpei Xia, Bing Ni, Huaizhi Wang","doi":"10.1007/s12032-024-02554-8","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Pancreatic ductal adenocarcinomas (PDAC) are huge threat to human for the extreme malignancy. PRIM2 was reported as tumor marker, while the functions and regulatory mechanisms in PDAC are still unclear. The study aimed to investigate the function of PRIM2 in PDAC.</p><p><strong>Methods: </strong>Expression was detected using immunohistochemistry (IHC), Western blot, and real-time quantitative PCR (RT-qPCR) methods. Cell assays and xenograft model confirmed the phenotypes. Co-Immunoprecipitation (Co-IP) and protein stability assays were used for protein interactions.</p><p><strong>Results: </strong>Inhibiting PRIM2 resulted in decreased proliferation and migration both in vitro and in vivo. PRIM2 upregulated FAM111B at increased RNA levels and protein stability.</p><p><strong>Conclusion: </strong>PRIM2/FAM111B axis promoted proliferation and migration by modulating the PI3K/AKT and epithelial-mesenchymal transition (EMT) markers. The axis has the potential to be targeted for PDAC treatment.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"6"},"PeriodicalIF":2.8000,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s12032-024-02554-8","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Pancreatic ductal adenocarcinomas (PDAC) are huge threat to human for the extreme malignancy. PRIM2 was reported as tumor marker, while the functions and regulatory mechanisms in PDAC are still unclear. The study aimed to investigate the function of PRIM2 in PDAC.
Methods: Expression was detected using immunohistochemistry (IHC), Western blot, and real-time quantitative PCR (RT-qPCR) methods. Cell assays and xenograft model confirmed the phenotypes. Co-Immunoprecipitation (Co-IP) and protein stability assays were used for protein interactions.
Results: Inhibiting PRIM2 resulted in decreased proliferation and migration both in vitro and in vivo. PRIM2 upregulated FAM111B at increased RNA levels and protein stability.
Conclusion: PRIM2/FAM111B axis promoted proliferation and migration by modulating the PI3K/AKT and epithelial-mesenchymal transition (EMT) markers. The axis has the potential to be targeted for PDAC treatment.
期刊介绍：
Medical Oncology (MO) communicates the results of clinical and experimental research in oncology and hematology, particularly experimental therapeutics within the fields of immunotherapy and chemotherapy. It also provides state-of-the-art reviews on clinical and experimental therapies. Topics covered include immunobiology, pathogenesis, and treatment of malignant tumors.
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