ArticleMedical oncology (Northwood, London, England)2015
FBXW7 overexpression suppresses renal cancer cell proliferation and induces apoptosis.
Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- FBXW7 induces apoptosis of nucleus pulposus cells to mediate intervertebral disc degeneration by regulating JNK expression.Journal of orthopaedic surgery and research · 2026Article
- FBXW7/GSK3β-mediated proline-rich 11 degradation promotes oxidative DNA damage and inhibits tumor progression in renal cell carcinoma.Theranostics · 2025Article
- Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024Review
- Pan-cancer analysis of FBXW family with potential implications in prognosis and immune infiltration.Frontiers in immunology · 2022Article
- Astragalus polysaccharides inhibit ovarian cancer cell growth via microRNA-27a/FBXW7 signaling pathway.Bioscience reports · 2020Article
- FBXW7 in Cancer: What Has Been Unraveled Thus Far?Cancers · 2019Review
- FBXW7: a critical tumor suppressor of human cancers.Molecular cancer · 2018Review
- Fbxw7 regulates renal cell carcinoma migration and invasion via suppression of the epithelial-mesenchymal transition.Oncology letters · 2018Article
- Upregulation of FBXW7 Suppresses Renal Cancer Metastasis and Epithelial Mesenchymal Transition.Disease markers · 2017Article
- Review
- MiR-27a-3p promotes esophageal cancer cell proliferation via F-box and WD repeat domain-containing 7 (FBXW7) suppression.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FBXW7 gene (F-box and WD-40 domain protein 7) is also named HCDC4 and is a significant tumor suppressor gene, which can regulate human cell cycle, proliferation and differentiation. In this study, we tend to investigate protein expression and related biological functions of FBXW7 gene. FBXW7 expression level in renal cell carcinoma (RCC) tissues is highly related to its clinical pathologic grade (P = 0.0094) and TNM phase (P = 0.0080) and is highly lower than in paracancerous normal tissues through immunohistochemistry study. FBXW7 high-expression patients have overall better prognosis than low-expression patients (P < 0.001). After transfected with FBXW7 plasmid, the RCC cell lines ACHN and A704 showed a depressed proliferation activity and high proportion of apoptosis through CCK8, colony formation and flow cytometry assay studies. By Western blot analysis, expression of cell proliferation-activating protein c-Myc and c-Jun is downregulated in FBXW7 high-expression RCC compared with negative control. These data suggested that FBXW7 is a significant tumor suppressor gene in RCC.
Indexed as
Identifiers
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.