The family with sequence similarity 83 member (FAM83D) plays important role in the process of cell division as well as tumour progression. However, the role of FAM83D in tissue development was not well explored. Here, we assessed transcriptional levels of FAM83D and other possibly related genes in organs of mice at different ages and methylation level of FAM83D promoter. Our results indicate the trend of FAM83D expression in mouse testis, liver, lung and small intestine, and its relationship to CYCLINB1 and KI67. Finally, we found no effect of promoter methylation status on FAM83D expression during mice development.
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| http://dx.doi.org/10.1016/j.gep.2021.119199 | DOI Listing |
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FAM83D promotes the progression of 4NQO-induced esophageal carcinoma via inhibiting FBWX7.
Exp Cell Res
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Department of Infection Management, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050011, PR China. Electronic address:
The present study aimed to explore the expression and regulatory role of FAM83D in the different developmental stages of esophageal squamous cell carcinoma (ESCC) to determine the effect of FAM83D on the proliferation, migration, and invasion of ESCC cells and to elucidate its underlying molecular mechanism. Immunohistochemistry (IHC) analysis revealed that the expression of FAM83D was obviously elevated in ESCC tissues compared to adjacent normal tissues. Furthermore, the FAM83D levels was positively correlated with tumor size, TNM stage, T stage, and N stage, while it was negatively correlated with FBXW7 expression, Karnofsky Performance Status (KPS) score, and survival rate.
View Article and Find Full Text PDFSEPT9: From pan-cancer to lung squamous cell carcinoma.
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Translational Medicine Research Center, Key Laboratory of Clinical Cancer Pharmacology and Toxicology Research of Zhejiang Province, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, 310006, Zhejiang, China.
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View Article and Find Full Text PDFFAM83D acts as an oncogene by regulating cell cycle progression via multiple pathways in synovial sarcoma: a potential novel downstream target oncogene of anlotinib.
Discov Oncol
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Department of Rheumatology and Immunology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200336, China.
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View Article and Find Full Text PDFThe FBXW7-binding sites on FAM83D are potential targets for cancer therapy.
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Key Laboratory Experimental Teratology of the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China.
Increasing evidence shows the oncogenic function of FAM83D in human cancer, but how FAM83D exerts its oncogenic function remains largely unclear. Here, we investigated the importance of FAM83D/FBXW7 interaction in breast cancer (BC). We systematically mapped the FBXW7-binding sites on FAM83D through a comprehensive mutational analysis together with co-immunoprecipitation assay.
View Article and Find Full Text PDFMETTL3 regulates FAM83D mA modification to accelerate tumorigenesis of triple-negative breast cancer via the Wnt/β-catenin pathway.
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Department of General Surgery, the First Affiliated Hospital of Jinzhou Medical University, Jinzhou 121000, China.
N6-methyladenosine (mA) modification, the most abundant methylation modification on eukaryotic mRNAs, was implicated in the tumourigenesis. This study aimed to explore the role of methyltransferase like 3 (METTL3) in triple-negative breast cancer progression and its underlying mechanisms. FAM83D was markedly elevated in triple-negative breast cancer tissues and cells, and high expression of FAM83D was related to the poor prognosis of triple-negative breast cancer patients.
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