ArticleCell metabolism2014
NCOA5, IL-6, type 2 diabetes, and HCC: The deadly quartet.
Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Identification and validation of NCOA5-ZCCHC3/FGF22 axis as a prognostic marker in lung adenocarcinoma migration and invasion.Cell death & disease · 2026Article
- NCOA5 induces sorafenib resistance in hepatocellular carcinoma by inhibiting ferroptosis.Cell death discovery · 2025Article
- Lifestyle factors, glycemic traits, and lipoprotein traits and risk of liver cancer: a Mendelian randomization analysis.Scientific reports · 2024Article
- Could NCOA5 a novel candidate gene for multiple sclerosis susceptibility?Molecular biology reports · 2023Article
- Hyperpolarization-activated cyclic nucleotide-gated cation channel 3 promotes HCC development in a female-biased manner.Cell reports · 2023Article
- Non-alcoholic fatty liver disease and diabetes mellitus as growing aetiologies of hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2023Review
- Insulin Inhibits Autophagy by Inhibiting the Binding of FoXO1 to the Promoter Region of GABARAPL1.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2023Article
- Expression and clinical significance of NCOA5 in epithelial ovarian cancer.Frontiers in oncology · 2023Article
- Article
- HnRNPU-AS1 inhibits the proliferation, migration and invasion of HCC cells and induces autophagy through miR-556-3p/ miR-580-3p/SOCS6 axis.Cancer biomarkers : section A of Disease markers · 2022Article
- Knockdown of NCOA5 suppresses viability, migration and epithelial-mesenchymal transition, and induces adhesion of breast cancer cells.Oncology letters · 2021Article
- Article
- NCOA5 Haplo-insufficiency Results in Male Mouse Infertility through Increased IL-6 Expression in the Epididymis.Scientific reports · 2019Article
- Matrine prevents the early development of hepatocellular carcinoma like lesions in rat liver.Experimental and therapeutic medicine · 2019Article
- Association between expression of nuclear receptor co-activator 5 protein and prognosis in postoperative patients with osteosarcoma.Oncology letters · 2018Article
- Overexpression of LBH is associated with poor prognosis in human hepatocellular carcinoma.OncoTargets and therapy · 2018Article
- A novel tumor suppressor geneOncoTargets and therapy · 2018Article
- NCOA5 promotes proliferation, migration and invasion of colorectal cancer cells via activation of PI3K/AKT pathway.Oncotarget · 2017Article
- A single non-synonymous NCOA5 variation in type 2 diabetic patients with hepatocellular carcinoma impairs the function of NCOA5 in cell cycle regulation.Cancer letters · 2017Article
- CCAT1 promotes hepatocellular carcinoma cell proliferation and invasion.International journal of clinical and experimental pathology · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although type 2 diabetes (T2D) is an established risk factor for hepatocellular carcinoma (HCC), the underlying mechanism that connects these two diseases is unknown. Gao et al. (2013) now suggest that nuclear receptor coactivator 5 (NCOA5) provides a genetic link between the two diseases through its effects on hepatic IL-6 expression.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.