DDIAS

Official Full Name

DNA damage induced apoptosis suppressor

Organism

Homo sapiens

GeneID

220042

Background

Involved in negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage and regulation of DNA stability. Predicted to be active in cytoplasm and nucleus. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

noxin; C11orf82;

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Detailed Information

The DDIAS (DNA damage-induced apoptosis suppressor) gene has garnered significant attention in recent years due to its pivotal role in regulating apoptosis and DNA damage response pathways. This article delves into the function, regulation, and implications of the DDIAS gene in cancer development and therapeutics.

Apoptosis, or programmed cell death, is a fundamental process in maintaining tissue homeostasis and eliminating abnormal or damaged cells. Dysregulation of apoptosis is a common hallmark of cancer, allowing tumor cells to evade apoptosis and proliferate indefinitely. The DDIAS gene, initially identified as a potential regulator of apoptosis, has emerged as a critical player in the DNA damage response and apoptosis suppression.

Function of DDIAS

The DDIAS gene encodes a protein that functions as a negative regulator of apoptosis. It interacts with key apoptosis regulators, such as Bcl-2 and Bcl-xL, and inhibits their pro-apoptotic function. Additionally, DDIAS protein binds to and stabilizes p53, a tumor suppressor protein that plays a crucial role in the DNA damage response. By inhibiting p53 ubiquitination and degradation, DDIAS enhances its stability and activity, promoting cell survival in response to DNA damage.

Regulation of DDIAS

DDIAS expression is tightly regulated at multiple levels, including transcriptional, post-transcriptional, and post-translational mechanisms. Several transcription factors, such as NFATc1 and CREB, have been shown to bind to the DDIAS promoter and regulate its expression. Moreover, miRNAs, small non-coding RNAs that regulate gene expression, have also been implicated in the post-transcriptional regulation of DDIAS. These regulatory mechanisms ensure that DDIAS expression is finely tuned to maintain a balance between apoptosis and cell survival.

Fig1. Regulation of DDIAS expression

Implications in Cancer Development and Therapeutics

Given its role in suppressing apoptosis and stabilizing p53, the DDIAS gene is of significant interest in cancer research. Elevated DDIAS expression has been observed in various cancer types, including breast, lung, and colon cancers, and is associated with tumor progression and poor prognosis. Conversely, downregulation of DDIAS has been shown to enhance the sensitivity of cancer cells to DNA-damaging agents, indicating its potential as a therapeutic target.

Strategies to Target DDIAS in Cancer Therapy

In recent years, efforts have been made to develop targeted therapies against the DDIAS gene. Small molecules that inhibit DDIAS activity have been identified and shown to potentiate the effects of DNA-damaging agents in vitro and in vivo. Additionally, novel therapeutic approaches, such as RNA interference (RNAi) and CRISPR/Cas9 gene editing, are being explored to knockout or silence DDIAS expression in cancer cells.

References:

Im JY, Kang MJ, Kim BK, Won M. DDIAS, DNA damage-induced apoptosis suppressor, is a potential therapeutic target in cancer. Exp Mol Med. 2023 May;55(5):879-885. doi: 10.1038/s12276-023-00974-6. Epub 2023 May 1. PMID: 37121974; PMCID: PMC10238375.
Im JY, Kim BK, Lee JY, Park SH, Ban HS, Jung KE, Won M. DDIAS suppresses TRAIL-mediated apoptosis by inhibiting DISC formation and destabilizing caspase-8 in cancer cells. Oncogene. 2018 Mar;37(9):1251-1262. doi: 10.1038/s41388-017-0025-y. Epub 2017 Dec 15. PMID: 29242605.

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