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Last update 08 May 2025

DEPDC1

Last update 08 May 2025

Basic Info

Synonyms

DEP domain containing 1, DEP domain-containing protein 1A, DEP.8

+ [4]

Introduction

May be involved in transcriptional regulation as a transcriptional corepressor. The DEPDC1A-ZNF224 complex may play a critical role in bladder carcinogenesis by repressing the transcription of the A20 gene, leading to transport of NF-KB protein into the nucleus, resulting in suppression of apoptosis of bladder cancer cells.

Drugs associated with DEPDC1

Asudemotide

Target

DEPDC1 x IGF2BP3 x KIF20B x LY6K x NUF2

Mechanism

DEPDC1 inhibitors [+4]

Active Org.

OncoTherapy Science, Inc.

Originator Org.

OncoTherapy Science, Inc.

Active Indication

Esophageal Carcinoma [+2]

Inactive Indication-

Drug Highest PhasePhase 3

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with DEPDC1

JPRN-UMIN000023324

/ CompletedPhase 1

Exploratory study to determine S-588410-induced tumor infiltrating lymphocytes and changes in the tumor microenvironment in esophageal cancer patients - Exploratory study to determine S-588410-induced tumor infiltrating lymphocytes and changes in the tumor microenvironment in esophageal cancer patients

Start Date25 Jul 2016

Sponsor / Collaborator

Shionogi & Co., Ltd.

JPRN-UMIN000016954

/ CompletedPhase 3

A multicenter, randomized, double-blind, placebo-controlled, phase 3 study of S-588410 as adjuvant therapy after curative resection in patients with esophageal cancer - A multicenter, randomized, double-blind, placebo-controlled, phase 3 study of S-588410 as adjuvant therapy after curative resection in patients with esophageal cancer

Start Date01 May 2015

Sponsor / Collaborator

Shionogi & Co., Ltd.

NCT02410369

/ Unknown statusPhase 2IIT

Phase II Study of S-588410 as Maintenance Monotherapy After Adjuvant Chemotherapy in Patients With Completely Resected Non-small- Cell Lung Cancer

In this clinical study, the investigators evaluate the efficacy and safety of S-588410 in patients who underwent an adjuvant chemotherapy after the complete resection of non-small-cell lung cancer.

Start Date01 Mar 2015

Sponsor / Collaborator

University of Tokyo

[+5]

100 Clinical Results associated with DEPDC1

100 Translational Medicine associated with DEPDC1

0 Patents (Medical) associated with DEPDC1

116

Literatures (Medical) associated with DEPDC1

01 Feb 2025·Expert Review of Hematology

Exploring shared pathogenesis of multiple myeloma and osteoporosis via bioinformatic analysis

Article

Author: Ma, Yiming ; Tang, Kegong ; Wang, Yajie ; Liu, Chengdi ; Li, Xiaofei ; Liu, Xinran ; Zhang, Jiyun

BACKGROUNDThe purpose of this study is to explore the common differentially expressed genes (DEGs) between multiple myeloma (MM) and osteoporosis and the associated molecular mechanisms.RESEARCH DESIGN AND METHODSWe obtained the overlapping DEGs between MM and osteoporosis with the GEO2R online tool. Then, the DEGs were clustered on the MetaCore website to identify the biological process and pathway. In addition, the STRING database and Cytoscape were used to construct the protein-protein interaction (PPI) network and identify hub genes. Finally, miRNA-gene and transcriptional factor (TF)-gene interaction networks were constructed.RESULTSA total of 252 genes were identified as DEGs in the overlapping two datasets. Functional analysis emphasizes the crucial role of the cell cycle in these two diseases. 10 hub genes were identified using cytoHubba, including CCNA2, ASPM, MKI67, FN1, FEN1, STAT1, DEPDC1, ITGB8, DYNC2LI1, HBEGF. In addition, according to the miRNA-gene and TF-gene interaction networks, part of TFs (RELA, TP53), and miRNAs (miR-26b-5p, miR-192-5p) may be identified as key regulators in MM and osteoporosis at the same time.CONCLUSIONSThe present study reveals the common pathogenesis of MM and osteoporosis. These shared pathways may provide new targets for further mechanistic studies of the pathogenesis and treatment of MM and osteoporosis.

01 Feb 2025·Cancer Biomarkers

Biomarkers and potential function analysis of triple-negative breast cancer screening based on bioinformatics

Article

Author: Li, Dan ; Yang, Yang ; Wang, Xiaoli ; Guo, Wenjia ; Chen, Lin ; Zhou, Duanfang ; Tan, Xiaodan ; Chen, Xing ; Peng, Zhe

This study aims to identify and validate potential endogenous biomarkers for triple-negative breast cancer (TNBC). TNBC microarray data (GSE38959, GSE53752) were retrieved from the Gene Expression Omnibus (GEO) database, and principal component analysis (PCA) was performed to evaluate the reliability of the data. The microarray datasets were merged, and differentially expressed genes (DEGs) were identified using R software. Functional enrichment analysis of the DEGs was conducted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The most disease-relevant module was identified through Weighted Gene Co-expression Network Analysis (WGCNA), and genes within this module were intersected with the DEGs. The intersecting genes underwent Least Absolute Shrinkage and Selection Operator (LASSO) regression analysis to minimize errors and identify TNBC-specific genes. Sensitivity and survival analyses were performed on the identified specific genes. There were 10 TNBC-specific genes identified: RRM2, DEPDC1, FIGF, TACC3, E2F1, CDO1, DST, MCM4, CHEK1, and PLSCR4. RT-qPCR analysis showed significant upregulation of CDO1, MCM4, DEPDC1, RRM2, and E2F1 in MDA-MB-231, CAL-148, and MFM-223 compared to MCF-10A. Our findings provide new insights into TNBC pathogenesis and potential therapeutic strategies, with important clinical implications for further understanding TNBC mechanisms and developing innovative treatments.

01 Nov 2024·Anti-Cancer Drugs

DEPDC1 affects autophagy-dependent glycolysis levels in human osteosarcoma cells by modulating RAS/ERK signaling through TTK

Article

Author: Xiao, Weiping ; Liu, Bailian ; Yu, Dong ; Li, Yingchun ; Chen, Lin

The current treatment for osteosarcoma (OS) is based on surgery combined with systemic chemotherapy, however, gene therapy has been hypothesized to improve patient survival rates. The density-enhanced protein domain 1 protein (DEPDC1) functions as a crucial determinant in the advancement of OS, which is highly expressed in OS cells. The current study was designed to delve into the effect and mechanism of DEPDC1 and phosphotyrosine-picked threonine tyrosine kinase (TTK) in OS. The expression of DEPDC1 and TTK in OS cells was detected by western blotting. Furthermore, the assessment of glycolysis encompassed the quantification of extracellular acidification rate, glucose uptake rate, lactate concentration, and the expression of glucose transporter 1, hexokinase 2, and pyruvate kinase M2. Finally, the functions of DEPDC1 and TTK in autophagy and ras-extracellular signal-regulated kinase signaling were determined by western blotting after interfering with DEPDC1 in SaOS-2 cells. The results revealed that DEPDC1 and TTK were upregulated in OS cell lines and interfering with DEPDC1 inhibited glycolysis and autophagy in OS cells. Furthermore, the STRING database suggested that DEPDC1 and TTK perform targeted binding. Notably, the results of the present study revealed that DEPDC1 upregulated RAS expression through TTK and enhanced ERK activity, thereby affecting glycolysis and autophagy in OS cells. Collectively, the present investigation demonstrated that DEPDC1 affected autophagy-dependent glycolysis levels of OS cells by regulating RAS/ERK signaling through TTK.

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DEPDC1

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