| Study (first author year) | Publication date | System/model | Main finding about FBXO8 | Quantitative/statistical highlights | Relevance (molecular function/localization/disease) | URL/DOI |
|---|---|---|---|---|---|---|
| Wang 2013 | 2013-06-27 | Human hepatocellular carcinoma (HCC): 120 paraffin-embedded cases, 20 matched fresh tissues, 5 HCC cell lines, mouse xenograft/metastasis assays | Verified identity as human FBX8/FBXO8, an F-box protein with a putative Sec7 domain; reports prior evidence that FBX8 is a Skp1-binding protein with E3 ligase activity toward ARF6, and experimentally shows FBXO8 acts as a suppressor of HCC proliferation, migration, invasion, tumor growth, and lung metastasis. FBXO8 was downregulated in HCC tissues/cell lines and was an independent prognostic factor for survival. (pqac-00000006, pqac-00000007) | 83/106 HCC samples (78.3%) showed low FBX8 expression vs 23/106 (21.7%) high expression; lower FBX8 associated with worse 5-year survival (Kaplan-Meier, P=0.002); expression lower in HCC vs adjacent liver/cirrhotic liver (both P<0.001); correlation with differentiation (P=0.008) and serum AFP (P=0.005); in tail-vein metastasis model, lung metastasis in 67% (4/6) mock vs 17% (1/6) FBX8-overexpressing mice; fewer metastatic lung nodules and smaller tumors with FBX8 overexpression (P<0.05). (pqac-00000006, pqac-00000007, pqac-00000009, pqac-00000010) | Disease evidence strongest in HCC; supports tumor-suppressive role. Also anchors molecular-function discussion by linking FBXO8 to SCF/Skp1 and prior ARF6 ubiquitination literature. | https://doi.org/10.1371/journal.pone.0065495 |
| Lu & Pfeffer 2014 | 2014-07 | Review of secretory-pathway Cullin-RING ligases | Review states that the SCF substrate receptor FBXO8 binds ARF6 via its Sec7 domain, localizes to the plasma membrane via its Sec7 and F-box domains, and mediates ARF6 ubiquitination; places FBXO8 at the interface of membrane trafficking and ubiquitin signaling. (pqac-00000001) | Review-level statement; no primary numerical data in the retrieved excerpt. (pqac-00000001) | Key for inferred subcellular localization (plasma membrane) and mechanistic hypothesis that FBXO8 regulates ARF6-dependent trafficking/invasive behavior rather than acting as a canonical Sec7 GEF. | https://doi.org/10.1016/j.tcb.2014.02.001 |
| Hundley 2021 | 2021-03-18 | Human HAP1 CRISPR-Cas9 ubiquitin-pathway screen across 41 compounds | Genome-scale chemical-genetic screen found that loss of FBXO8 renders cells resistant to the vesicular transport inhibitor brefeldin A, a phenotype noted as consistent with FBXO8 containing a Sec7-like domain. This is functional-genetic, not direct biochemical proof of GEF activity. (pqac-00000000) | Global screen uncovered 466 gene-compound interactions covering 25% of interrogated E3s/DUBs; FBXO8 signal was specifically highlighted as brefeldin A resistance in the tool-derived relevant snippet, but no FBXO8-specific effect size was provided in the retrieved text. (pqac-00000000, pqac-00000005) | Supports a trafficking-related role and compatibility of FBXO8 domain architecture with Golgi/ARF pathway biology; evidence is indirect and should not be overinterpreted as direct Sec7 catalytic activity. | https://doi.org/10.1016/j.molcel.2021.01.014 |
| Zhang 2022 | 2022-01-03 | Public-database analysis of FBXO family in pancreatic ductal adenocarcinoma (PDAC) | Establishes general context that FBXO proteins are substrate-recognition subunits of SCF E3 ligases involved in cancer pathways; notes that some FBXO members including FBXO8 have limited PDAC-focused study. In this paper, FBXO8 itself was not one of the six prioritized PDAC FBXOs. (pqac-00000003) | Six prioritized FBXOs showed >40% genetic alterations/mutations in PDAC and associations with prognosis/immune infiltration, but these quantitative results were not FBXO8-specific. (pqac-00000003) | Useful family-level context for current understanding of FBXO8 as an SCF-type substrate receptor; does not provide direct mechanistic FBXO8 evidence. | https://doi.org/10.3389/fimmu.2021.774435 |
| Gelman 2023 | 2023-03 | Review of metastatic dormancy genomics | Review-level claim states FBXO8 is an example of a protein that promotes dormancy by upregulating EMT and stem-like markers; this should be treated cautiously because it contrasts with the suppressor-of-invasion framing from HCC studies and the retrieved excerpt does not provide primary supporting data. (pqac-00000008, pqac-00000000) | No quantitative FBXO8-specific statistics in the retrieved excerpt. (pqac-00000008) | Potentially relevant to metastasis/dormancy biology, but currently lower-confidence than HCC experimental evidence; highlights context dependence and need to verify underlying primary source before strong annotation. | https://doi.org/10.1007/s10555-022-10076-w |
| Open Targets summary | Accessed from current Open Targets snapshot in tool output (date not stated in output) | Curated disease-target evidence aggregation for human FBXO8/ENSG00000164117 | Open Targets lists low-to-moderate evidence links between FBXO8 and several diseases/phenotypes, with supporting literature/study IDs rather than mechanistic annotation. Top listed associations in the retrieved output were actinic keratosis, neurodegenerative disease, pericarditis, precordial pain, and cataract. (pqac-00000000) | Evidence sizes were 2 for each listed disease in the retrieved output; example association scores: neurodegenerative disease 0.231, precordial pain 0.171, cataract 0.167, pericarditis 0.128, actinic keratosis 0.127. Supporting literature IDs in the output included PMID 34031600 and PMID 39024449. (pqac-00000000) | Helpful for disease landscape scanning, but evidence is indirect/aggregated and does not itself define molecular function or localization. | https://platform.opentargets.org/target/ENSG00000164117 |


*Table: This table compiles the most relevant retrieved evidence for human FBXO8/Q9NRD0, separating direct experimental findings from review-level or database-level inferences. It is useful for distinguishing well-supported roles in ARF6-related trafficking and cancer suppression from more tentative disease associations and recent contextual claims.*