ArticleOncogene2020
CBX7 binds the E-box to inhibit TWIST-1 function and inhibit tumorigenicity and metastatic potential.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 46 citations in OpenAlex.
- Structural landscape of H3K27me3 recognition by protein domains and their potential for inhibition.The Journal of biological chemistry · 2026Review
- DNMT1-Induced Downregulation of CBX7 Inhibits ERK Phosphorylation and Promotes Pancreatic Ductal Adenocarcinoma Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Unravelling the impact of the chromobox proteins in human cancers.Cell death & disease · 2025Review
- Epigenetic regulation by polycomb repressive complex 1 promotes cerebral cavernous malformations.EMBO molecular medicine · 2024Article
- Ribosomal proteins in hepatocellular carcinoma: mysterious but promising.Cell & bioscience · 2024Review
- Article
- Review
- Review
- Adipose-derived exosomal miR-421 targets CBX7 and promotes metastatic potential in ovarian cancer cells.Journal of ovarian research · 2023Article
- Adipose-derived exosomal miR-421 targets CBX7 and promotes metastatic potential in ovarian cancer cells.bioRxiv : the preprint server for biology · 2023Article
- A Novel Role of Connective Tissue Growth Factor in the Regulation of the Epithelial Phenotype.Cancers · 2023Article
- Article
- Chromobox proteins in cancer: Multifaceted functions and strategies for modulation (Review).International journal of oncology · 2023Review
- Generation of Stable Epithelial-Mesenchymal Hybrid Cancer Cells with Tumorigenic Potential.Cancers · 2023Article
- TWIST1 induces proteasomal degradation of β-catenin during the differentiation of ovarian cancer stem-like cells.Scientific reports · 2022Article
- Epithelial-Mesenchymal Transition-Mediated Tumor Therapeutic Resistance.Molecules (Basel, Switzerland) · 2022Review
- Liver-specific deletion of miR-181ab1 reduces liver tumour progression via upregulation of CBX7.Cellular and molecular life sciences : CMLS · 2022Article
- Expression profile and prognostic values of Chromobox family members in human glioblastoma.Aging · 2022Article
- Prognostic Value and Therapeutic Potential of CBX Family Members in Ovarian Cancer.Frontiers in cell and developmental biology · 2022Article
- Identification and Validation of Chromobox Family Members as Potential Prognostic Biomarkers and Therapeutic Targets for Human Esophageal Cancer.Frontiers in genetics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Deaths from ovarian cancer usually occur when patients succumb to overwhelmingly numerous and widespread micrometastasis. Whereas epithelial-mesenchymal transition is required for epithelial ovarian cancer cells to acquire metastatic potential, the cellular phenotype at secondary sites and the mechanisms required for the establishment of metastatic tumors are not fully determined. Using in vitro and in vivo models we show that secondary epithelial ovarian cancer cells (sEOC) do not fully reacquire the molecular signature of the primary epithelial ovarian cancer cells from which they are derived. Despite displaying an epithelial morphology, sEOC maintains a high expression of the mesenchymal effector, TWIST-1. TWIST-1 is however transcriptionally nonfunctional in these cells as it is precluded from binding its E-box by the PcG protein, CBX7. Deletion of CBX7 in sEOC was sufficient to reactivate TWIST-1-induced transcription, prompt mesenchymal transformation, and enhanced tumorigenicity in vivo. This regulation allows secondary tumors to achieve an epithelial morphology while conferring the advantage of prompt reversal to a mesenchymal phenotype upon perturbation of CBX7. We also describe a subclassification of ovarian tumors based on CBX7 and TWIST-1 expression, which predicts clinical outcomes and patient prognosis.
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.