ArticleBiochemical genetics2026
Transcription Activation of DEPDC1B Upon EBF1 Loss Contributes to Cell Cycle Progression and Epithelial-Mesenchymal Transition in Colon Adenocarcinoma.
Article in Biochemical genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- EBF1 Deficiency Drives Prostate Cancer Progression by Interfering with the Transcriptional Regulation ofOncology research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Grounded on bioinformatics insights, this study investigates the interaction between DEP domain containing 1B (DEPDC1B) and early B cell factor 1 (EBF1), their expression patterns, and their functions in the progression of colon adenocarcinoma (COAD). DEPDC1B was identified as a potential oncogene aberrantly expressed in COAD, and its high expression was detected in COAD cell lines. DEPDC1B silencing in COAD cell lines while blocking epithelial-mesenchymal transition (EMT), dissemination, and expansion of COAD cells in vitro. Additionally, DEPDC1B knockdown suppressed tumorigenic activity and metastasis of mouse CT26 cells in isograft tumor models. EBF1, poorly expressed in COAD, was found to repress DEPDC1B transcription. EBF1 overexpression reduced DEPDC1B expression, thus diminishing the malignant properties of cancer cells. Nevertheless, its tumor-suppressive effects were negated by DEPDC1B restoration. EBF1 presented a promoter hypermethylation pattern in COAD cell lines, in which its expression was restored upon treatment of the methylation inhibitor 5-azacytidine. In conclusion, this study highlights that the hypermethylation of EBF1 leads to transcription activation of DEPDC1B, which promotes cell cycle progression, EMT, and malignant progression in COAD. Restoring EBF1 levels or suppressing DEPDC1B expression may be promising strategies for COAD management.
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.