{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n FAM83F, a member of the FAM83 family defined by a conserved DUF1669 domain, has emerged as an important modulator of oncogenic signaling in multiple cancer types. In esophageal squamous cell carcinoma (ESCC), studies revealed that FAM83F expression is negatively regulated by microRNAs such as miR‐455‐3p and miR‐143, with forced miRNA expression leading to reduced proliferation and invasion – underscoring a tumor‐suppressive impact when FAM83F levels are diminished."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In lung cancers, including non‐small cell lung cancer (NSCLC) and lung adenocarcinoma, FAM83F appears to function in an oncogenic capacity. Its overexpression—regulated by microRNAs such as miR‐940, miR‐1827, and modulated via competing endogenous RNAs (for example, circ_0000735 sponging miR‐635)—promotes cell viability, proliferation, migration, and invasion."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "5"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In glioma, reduced levels of miR‐650 correlate with elevated FAM83F expression and enhanced cellular proliferation, further supporting its tumor‐promoting role in certain contexts."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond its role in promoting proliferation and invasion, FAM83F is also involved in the regulation of critical signaling pathways. One study demonstrated that FAM83F interacts with p53, reducing its ubiquitination and degradation to stabilize and enhance p53 activity in response to DNA damage—even in cells harboring mutant p53, where it additionally influences migratory behavior."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In colorectal cancer cells, immunomodulatory imide drugs (IMiDs) were shown to induce degradation of FAM83F, which in turn attenuates canonical Wnt signaling via displacement of CK1α from the plasma membrane."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In papillary thyroid cancer, overexpression of FAM83F with a distinct cytoplasmic localization further supports its involvement as a biomarker in tumor progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n At the molecular level, the conserved DUF1669 domain of FAM83F facilitates its interaction with various CK1 isoforms, positioning FAM83F as a regulator of subcellular kinase localization and activity – a function that is shared by other FAM83 family members."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n More broadly, integrative genomic analyses have implicated the FAM83 family, including FAM83F, as key players in EGFR/RAS signaling and oncogenic transformation. Elevated expression of these proteins is associated with enhanced tumorigenic signaling and poor clinical prognosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings indicate that FAM83F contributes to tumor progression by participating in diverse signaling networks—ranging from the regulation of p53 and Wnt pathways to the modulation of kinase localization—thereby presenting itself as a potential therapeutic target and biomarker in multiple malignancies.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "H Yang, Y-N Wei, J Zhou, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "miR-143 inhibits tumor progression by targeting FAM83F in esophageal squamous cell carcinoma."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Tumour Biol (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s13277-015-4760-9"}], "href": "https://doi.org/10.1007/s13277-015-4760-9"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26758433"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26758433"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "G-M Gu, Y-Y Zhan, K Abuduwaili, et al. 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