ArticleCell cycle (Georgetown, Tex.)2016
p53 directly regulates the glycosidase FUCA1 to promote chemotherapy-induced cell death.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 33 citations in OpenAlex.
- L-Fucose: a dietary sugar with multifaceted potential in the biology and therapy of cancer.Nature reviews. Cancer · 2026Review
- The deubiquitinase USP35: from an oncogenic hub to a therapeutic target in human cancers.Frontiers in oncology · 2026Review
- Single-cell RNA sequencing and functional analysis reveal the role of altered glycosylation levels of hepatic macrophages in liver cirrhosis.Journal of gastroenterology · 2025Article
- CTCF-activated FUCA1 functions as a tumor suppressor by promoting autophagy flux and serum α-L-fucosidase serves as a potential biomarker for prognosis in ccRCC.Cancer cell international · 2024Article
- Construction and analysis of a lysosome-dependent cell death score-based prediction model for non-small cell lung cancer.Discover oncology · 2024Article
- Review
- p53 rapidly restructures 3D chromatin organization to trigger a transcriptional response.Nature communications · 2024Article
- Article
- The FBXW7-binding sites on FAM83D are potential targets for cancer therapy.Breast cancer research : BCR · 2024Article
- USP35 promotes cell proliferation and chemotherapeutic resistance through stabilizing FUCA1 in colorectal cancer.Oncogenesis · 2023Article
- The complexity of p53-mediated metabolic regulation in tumor suppression.Seminars in cancer biology · 2022Review
- Glycan degradation promotes macroautophagy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Dual role of fucosidase in cancers and its clinical potential.Journal of Cancer · 2022Review
- Downregulation of α-l-fucosidase 1 suppresses glioma progression by enhancing autophagy and inhibiting macrophage infiltration.Cancer science · 2020Article
- Roles of p53 Family Structure and Function in Non-Canonical Response Element Binding and Activation.International journal of molecular sciences · 2019Review
- Preoperative AFU Is a Useful Serological Prognostic Predictor for Colorectal Liver Oligometastasis Patients Undergoing Hepatic Resection.Journal of Cancer · 2019Article
- Reduced expression of α-L-Fucosidase-1 (FUCA-1) predicts recurrence and shorter cancer specific survival in luminal B LN+ breast cancer patients.Oncotarget · 2018Article
- Prognostic role of FUT8 expression in relation to p53 status in stage II and III colorectal cancer.PloS one · 2018Article
- Inhibition of coiled coil domain containing protein 69 enhances platinum-induced apoptosis in ovarian cancer cells.Oncotarget · 2017Article
- Census and evaluation of p53 target genes.Oncogene · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
p53 is a central factor in tumor suppression as exemplified by its frequent loss in human cancer. p53 exerts its tumor suppressive effects in multiple ways, but the ability to invoke the eradication of damaged cells by programmed cell death is considered a key factor. The ways in which p53 promotes cell death can involve direct activation or engagement of the cell death machinery, or can be via indirect mechanisms, for example though regulation of ER stress and autophagy. We present here another level of control in p53-mediated tumor suppression by showing that p53 activates the glycosidase, FUCA1, a modulator of N-linked glycosylation. We show that p53 transcriptionally activates FUCA1 and that p53 modulates fucosidase activity via FUCA1 up-regulation. Importantly, we also report that chemotherapeutic drugs induce FUCA1 and fucosidase activity in a p53-dependent manner. In this context, while we found that over-expression of FUCA1 does not induce cell death, RNAi-mediated knockdown of endogenous FUCA1 significantly attenuates p53-dependent, chemotherapy-induced apoptotic death. In summary, these findings add an additional component to p53s tumor suppressive response and highlight another mechanism by which the tumor suppressor controls programmed cell death that could potentially be exploited for cancer therapy.
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.