ArticleCell death and differentiation2021
FBXL6 degrades phosphorylated p53 to promote tumor growth.
Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 32 citations in OpenAlex.
- Elevated FBXL6 activates both wild-type KRAS and mutant KRASMilitary Medical Research · 2023Trial
- FBXL6 promotes bladder cancer progression by stabilizing ENO1 through K63-linked ubiquitination.Cell death discovery · 2026Article
- Breast Cancer-Secreted DPP3 Promotes Lung Metastasis by Remodelling the Vascular Niche in Lung via the Rap1 Signalling Pathway.Journal of extracellular vesicles · 2025Article
- Regular versus Irregular Exercise Differentially Modulates Hippocampal-Hepatic Acetylcholine Flux to Coordinate Fear Memory Extinction and Liver Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- FBXO44 Regulates FOXP1 Degradation Through AURKA-Dependent Phosphorylation to Promote Colorectal Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- TRIM36 inhibits lung fibroblast activation and pulmonary fibrosis through the degradation of phospho-AKT1.iScience · 2025Article
- F-box proteins in cancer: from cancer cells to the tumor microenvironment.Cell communication and signaling : CCS · 2025Review
- Lactylation-driven transcriptional activation of FBXO33 promotes gallbladder cancer metastasis by regulating p53 polyubiquitination.Cell death & disease · 2025Article
- Construction of a circadian rhythm-related gene signature for predicting the prognosis and immune infiltration of breast cancer.Frontiers in molecular biosciences · 2025Article
- Significance of circular RNAs in regulating protein ubiquitination for malignant tumor progression.Frontiers in immunology · 2025Review
- The Clinical Prediction Value of the Ubiquitination Model Reflecting the Microenvironment Infiltration and Drug Sensitivity in Breast Cancer.Journal of Cancer · 2025Article
- Prognostic value and drug sensitivity of F‑box and leucine‑rich repeat protein 6 in glioma.Oncology letters · 2024Article
- Role of protein degradation systems in colorectal cancer.Cell death discovery · 2024Review
- Synthesis, characterization, and anti-cancer potential of novel p53-mediated Mdm2 and Pirh2 modulators: an integratedFrontiers in chemistry · 2024Article
- Article
- Deer antlers: the fastest growing tissue with least cancer occurrence.Cell death and differentiation · 2023Review
- F-box and leucine-rich repeat 6 promotes gastric cancer progressionWorld journal of gastrointestinal oncology · 2023Article
- Reprogramming of palmitic acid induced by dephosphorylation of ACOX1 promotes β-catenin palmitoylation to drive colorectal cancer progression.Cell discovery · 2023Article
- QSER1 preserves the suppressive status of the pro-apoptotic genes to prevent apoptosis.Cell death and differentiation · 2023Article
- FBXL6 is dysregulated in keloids and promotes keloid fibroblast growth by inducing c-Myc expression.International wound journal · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ubiquitin-proteasome system regulates many distinct biological processes. Its dysregulation causes various diseases, including but not limited to cancer. In this study, based on the analysis of gene expression in several colorectal cancer (CRC) datasets, we show that FBXL6, a poorly-characterized F-box protein, is amplified, over-expressed, and highly correlated with poor prognosis in human CRC patients. Mechanistically, FBXL6 targets phospho-p53 (S315) to mediate its polyubiquitination and proteasomal degradation, thereby inhibiting p53 signaling. FBXL6 depletion inhibits proliferation of p53 wild-type (WT) CRC cells by inducing cell cycle arrest and apoptosis. Furthermore, p53 transcriptionally suppresses FBXL6 expression by binding its core promoter region. Taken together, these results identify the feed-forward loop of FBXL6-p53 as a potential therapeutic target for CRC treatments.
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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.