Transcription Activation of DEPDC1B Upon EBF1 Loss Contributes to Cell Cycle Progression and Epithelial Mesenchymal Transition in Colon Adenocarcinoma

Sep 23, 2026

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Grounded on bioinformatics insights, this study investigates the interaction between DEPDC1B and EBF1, analyzing their expression patterns and functional roles in colon adenocarcinoma (COAD) progression. DEPDC1B is identified as a potential oncogene with aberrant high expression; silencing it blocks EMT, dissemination, and expansion in vitro and suppresses CT26 tumorigenicity and metastasis in isograft models. EBF1, poorly expressed in COAD, represses DEPDC1B transcription, and restoring EBF1 or inhibiting EBF1 promoter methylation reduces malignancy.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages20

Reading Time50 min

AccessFree to download

Abstract

Keywords

Introduction

Background on colorectal cancer and COAD progression

Hallmarks of cancer and the role of EMT

Rationale for DEPDC1B and EBF1 in COAD

Biochemical Genetics (2026) 64:5665–5684 [https://doi.org/10.1007/s10528-025-1](https://doi.org/10.1007/s10528-025-1)1307-9 ORIGINAL ARTICLE Transcription Activation of DEPDC1B Upon EBF1 Loss Contributes to Cell Cycle Progression and EpithelialMesenchymal Transition in Colon Adenocarcinoma Yang Li1 · Xin Shi1 · Baoyong Ling1 · Xiangyu Su2 · Jing Zhang1 Received: 23 April 2025 / Accepted: 27 November 2025 / Published online: 16 December 2025 © The Author(s) 2025 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, DEPDC1Bknockdown 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 maybe promising strategies for COAD management. Extended author information available on the last page of the article Graphical Abstract Keywords DEPDC1B · EBF1 · Cell cycle · EMT · COAD · Promoter methylation Introduction With approximately 1.93 million new diagnoses and the associated 903,859 deaths, colorectal cancer (CRC) ranked the third in overall incidence while the second in mortality across cancer types in 2022 (Bray et al. 2024). Among the various forms of CRC, colon adenocarcinoma (COAD) is the most prevalent, which refers to a malignant tumor that originates from the epithelial cells of the colon and features glandular differentiation (Liu et al. 2019). The progression of COAD typically follows a multistep process, beginning with normal mucosa, advancing to adenomas, and ultimately developing into carcinoma (Arnold et al. 2017; Mutch 2007) . While surgery offers a potential cure for early-stage CRC, patients with metastatic disease, which accounts for 25% of all diagnosed cases, currently have limited treatment options (Chou et al. 2022). The high mortality rate associated is primarily due to late-stage diagnosis and the cancer’s tendency to spread to distant organs (Hernandez Dominguez et al. 2023; Koncina et al. 2020; Sendi et al. 2022). The 5-year survival rate ranges significantly, from about 90% in stage I patients to just over 10% in those with stage IV disease (Miller et al. 2019; Siegel et al. 2020) . Identifying key oncogenes involved in tumor progression could open doors for new therapeutic strategies for COAD management. The development of tumors is characterized by several hallmarks, including unchecked cell proliferation, resistance to cell death, evasion of growth suppressors, limitless replication potential, angiogenesis, and the capacities to disseminate and metastasize (Hanahan and Weinberg 2011). One crucial process in tumor progression is epithelial-to-mesenchymal transition (EMT), which enables tumor cells to lose their cell-cell junctions, reduce expression of E-cadherin, and increase mesenchymal markers like vimentin and N-cadherin. EMT is a pivotal event that allows otherwise stationar

FAQs

What role does DEPDC1B play in colon adenocarcinoma progression?

DEPDC1B is proposed as an oncogene aberrantly expressed in COAD, and its silencing blocks EMT, dissemination, and tumor expansion in vitro.

How does EBF1 affect DEPDC1B transcription and cancer cell malignancy?

EBF1 represses DEPDC1B transcription; overexpression of EBF1 reduces DEPDC1B expression and diminishes malignant properties.

Why are promoter methylation and 5-azacytidine relevant to EBF1 in COAD?

EBF1 shows a promoter hypermethylation pattern in COAD cell lines, and its expression is restored after treatment with the methylation inhibitor 5-azacytidine.

Sep 23, 2026

Uploaded by moss~