Last update 19 Sep 2024

DEPDC1

Last update 19 Sep 2024

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

S-288310/S-488310

Target

DEPDC1 x KIF20B

Mechanism

DEPDC1 inhibitors [+1]

Active Org.

OncoTherapy Science, Inc. [+1]

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

108

Literatures (Medical) associated with DEPDC1

01 Aug 2024·International Journal of Biological Macromolecules

Exosomal miR-130b-3p suppresses metastasis of non-small cell lung cancer cells by targeting DEPDC1 via TGF-β signaling pathway

Article

Author: Yin, Zhihua ; Li, Xuelian ; Yang, He ; Lv, Meiwen ; Tian, Wen ; Zhou, Baosen ; Zheng, Chang

Exosomal miRNAs have vital functions in mediating intercellular communication as well as tumor occurrence and development. Thus, our research was aimed at exploring the regulatory mechanisms of exosomal miR-130b-3p/DEP domain containing 1 (DEPDC1)/transforming growth factor-β (TGF-β) signaling pathway in non-small cell lung cancer (NSCLC). Here we indicated that exosomal miR-130b-3p expression decreased in the serum of NSCLC patients, and it was of significant diagnostic value. Moreover, elevated miR-130b-3p levels suppressed the proliferation and migration of NSCLC cells, and enhanced their apoptosis. Conversely, miR-130b-3p down-regulation led to an opposite effect. As the upstream of DEPDC1, miR-130b-3p directly bound to 3'UTR in DEPDC1 to regulate its expression. DEPDC1 levels affected the proliferation, migration, and apoptosis of NSCLC cells via TGF-β signaling pathway. Exosomal miR-130b-3p was highly expressed in BEAS-2B cells, besides, BEAS-2B cells transferred exosomal miR-130b-3p to NSCLC cells. Finally, exosomal miR-130b-3p suppressed NSCLC cell growth and migration, promoted their apoptosis via TGF-β signaling pathway by decreasing DEPDC1 expression, and suppressed epithelial-mesenchymal transition (EMT) in NSCLC cells. In conclusion, exosomal miR-130b-3p has the potential to be a predictive biomarker for NSCLC, thereby stimulating the exploration of diagnostic and therapeutic approaches targeting NSCLC.

31 Jul 2024·Bioscience Reports

Retraction: DEPDC1 promotes cell proliferation and suppresses sensitivity to chemotherapy in human hepatocellular carcinoma

01 Jun 2024·Animal Models and Experimental Medicine

CircPMS1 promotes proliferation of pulmonary artery smooth muscle cells, pulmonary microvascular endothelial cells, and pericytes under hypoxia

Article

Author: Zhao, Qinhua ; Wei, Yaqin ; Zhao, Hui ; Wang, Lan ; Wu, Wenhui ; Duan, Ruowang ; Jiang, Rong ; Hu, Xiaoyi ; Wang, Shang ; Yuan, Ping ; Liu, Jinming ; Gong, Sugang

AbstractBackgroundCircular RNAs (circRNAs) have been recognized as significant regulators of pulmonary hypertension (PH); however, the differential expression and function of circRNAs in different vascular cells under hypoxia remain unknown. Here, we identified co‐differentially expressed circRNAs and determined their putative roles in the proliferation of pulmonary artery smooth muscle cells (PASMCs), pulmonary microvascular endothelial cells (PMECs), and pericytes (PCs) under hypoxia.MethodsWhole transcriptome sequencing was performed to analyze the differential expression of circRNAs in three different vascular cell types. Bioinformatic analysis was used to predict their putative biological function. Quantitative real‐time polymerase chain reaction, Cell Counting Kit‐8, and EdU Cell Proliferation assays were carried out to determine the role of circular postmeiotic segregation 1 (circPMS1) as well as its potential sponge mechanism in PASMCs, PMECs, and PCs.ResultsPASMCs, PMECs, and PCs exhibited 16, 99, and 31 differentially expressed circRNAs under hypoxia, respectively. CircPMS1 was upregulated in PASMCs, PMECs, and PCs under hypoxia and enhanced the proliferation of vascular cells. CircPMS1 may upregulate DEP domain containing 1 (DEPDC1) and RNA polymerase II subunit D expression by targeting microRNA‐432‐5p (miR‐432‐5p) in PASMCs, upregulate MAX interactor 1 (MXI1) expression by targeting miR‐433‐3p in PMECs, and upregulate zinc finger AN1‐type containing 5 (ZFAND5) expression by targeting miR‐3613‐5p in PCs.ConclusionsOur results suggest that circPMS1 promotes cell proliferation through the miR‐432‐5p/DEPDC1 or miR‐432‐5p/POL2D axis in PASMCs, through the miR‐433‐3p/MXI1 axis in PMECs, and through the miR‐3613‐5p/ZFAND5 axis in PCs, which provides putative targets for the early diagnosis and treatment of PH.

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DEPDC1

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