ArticleOncotarget2017
GSK-3β phosphorylation-dependent degradation of ZNF281 by β-TrCP2 suppresses colorectal cancer progression.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 16 citations in OpenAlex.
- Retraction: Crosstalk between ATF4 and MTA1/HDAC1 promotes osteosarcoma progression.Oncotarget · 2026Article
- Research Progress on the Role of Zinc Finger Protein in Colorectal Cancer.Cancer reports (Hoboken, N.J.) · 2025Review
- The involvement of E3 ubiquitin ligases in the development and progression of colorectal cancer.Cell death discovery · 2023Review
- Inhibition of the transcription factor ZNF281 by SUFU to suppress tumor cell migration.Cell death and differentiation · 2023Article
- ZNF281 Promotes Colon Fibroblast Activation in TGFβ1-Induced Gut Fibrosis.International journal of molecular sciences · 2022Article
- Association of FBXW11 levels with tumor development and prognosis in chondrosarcoma.Cancer biomarkers : section A of Disease markers · 2022Article
- Understanding the regulation of β-catenin expression and activity in colorectal cancer carcinogenesis: beyond destruction complex.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Review
- FBXW11 contributes to stem-cell-like features and liver metastasis through regulating HIC1-mediated SIRT1 transcription in colorectal cancer.Cell death & disease · 2021Article
- Long Non-Coding RNA CCAT2 Activates RAB14 and Acts as an Oncogene in Colorectal Cancer.Frontiers in oncology · 2021Article
- F-box proteins and cancer: an update from functional and regulatory mechanism to therapeutic clinical prospects.Theranostics · 2020Review
- CircAGFG1 sponges miR-203 to promote EMT and metastasis of non-small-cell lung cancer by upregulating ZNF281 expression.Thoracic cancer · 2019Article
- Transcription Factor ZNF281: A Novel Player in Intestinal Inflammation and Fibrosis.Frontiers in immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc finger protein 281 (ZNF281) has been recently shown to be critical for CRC progression. However, the immediate upstream regulators of ZNF281 remain unclear. Here we reported that the E3 ligase the β-transducin repeat-containing protein 2 (β-TrCP2) governs the ubiquitination and degradation of ZNF281. In human CRC specimens, endogenous β-TrCP2 were inversely correlated with ZNF281. Beta-TrCP2 reversed the phenotype of CRC cell with overexpressed ZNF281. Moreover, we found that glycogen synthase kinase 3β (GSK-3β), not GSK-α, could bind to and phosphorylate ZNF281 at one consensus motif (TSGEHS; phosphorylation site is shown in italics), which promotes the interaction of ZNF281 with β-TrCP2, not β-TrCP1, and leads to the subsequent ubiquitination and degradation of phosphorylated ZNF281. A mutant of ZNF281 (ZNF281-S638A) is much more stable than wild-type ZNF281 because ZNF281-S638A mutant abolishes the phosphorylation by GSK-3β and can not be ubiquitinated and degraded by β-TrCP2. Conversely, ZNF281 transcriptionally repressed the expression of β-TrCP2, indicating a negative feedback loop between ZNF281 and β-TrCP2 in CRC cells. These findings suggest that the turnover of ZNF281 by β-TrCP2 might provide a potentially novel treatment for patients with CRC.
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.