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Last update 23 Jan 2025

GADD45B

Last update 23 Jan 2025

Basic Info

Synonyms

DKFZP566B133, GADD45B, GADD45BETA

+ [5]

Introduction

Involved in the regulation of growth and apoptosis. Mediates activation of stress-responsive MTK1/MEKK4 MAPKKK.

Drugs associated with GADD45B

KES-0001

Target

GADD45B

Mechanism

GADD45B inhibitors [+1]

Active Org.-

Originator Org.

Imperial College London

Active Indication-

Inactive Indication

Diffuse Large B-Cell Lymphoma [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GADD45B

100 Translational Medicine associated with GADD45B

0 Patents (Medical) associated with GADD45B

499

Literatures (Medical) associated with GADD45B

01 Feb 2025·Journal of Advanced Research

DNA hypomethylation-mediated upregulation of GADD45B facilitates airway inflammation and epithelial cell senescence in COPD

Article

Author: Yang, Ruonan ; Gu, Yiya ; Xie, Jungang ; Peng, Maocuo ; Chen, Shanshan ; Zhang, Jiaheng ; Deng, Zhesong ; Zhan, Yuan ; Zeng, Zhilin ; Zhang, Yating ; Wu, Jixing ; Huang, Qian

INTRODUCTIONChronic obstructive pulmonary disease (COPD) is a heterogeneous disease typically characterized by chronic airway inflammation, with emerging evidence highlighting the driving role of cellular senescence-related lung aging. Accelerated lung aging and inflammation mutually reinforce each other, creating a detrimental cycle that contributes to disease progression. Growth arrest and DNA damage-inducible (GADD45) family has been reported to involve in multiple biological processes, including inflammation and senescence. However, the role of GADD45 family in COPD remains elusive.OBJECTIVESTo investigate the role and mechanism of GADD45 family in COPD pathogenesis.METHODSExpressions of GADD45 family were evaluated by bioinformatic analysis combined with detections in clinical specimens. The effects of GADD45B on inflammation and senescence were investigated via constructing cell model with siRNA transfection or overexpression lentivirus infection and animal model with Gadd45b knockout. Targeted bisulfite sequencing was performed to probe the influence of DNA methylation in GADD45B expression in COPD.RESULTSGADD45B expression was significantly increased in COPD patients and strongly associated with lung function, whereas other family members presented no changes. GADD45B upregulation was confirmed in mice exposed by cigarette smoke (CS) and HBE cells treated by CS extract as well. Moreover, experiments involving bidirectional modulation of GADD45B expression in HBE cells further substantiated its positive regulatory role in inflammatory response and cellular senescence. Mechanically, GADD45B-facilitated inflammation was directly mediated by p38 phosphorylation, while GADD45B interacted with FOS to promote cellular senescence in a p38 phosphorylation-independent manner. Furthermore, Gadd45b deficiency remarkably alleviated inflammation and senescence of lungs in CS-exposed mice, as well as improved emphysema and lung function. Eventually, in vivo and vitro experiments demonstrated that GADD45B overexpression was partially mediated by CS-induced DNA hypomethylation.CONCLUSIONOur findings have shed light on the impact of GADD45B in the pathogenesis of COPD, thereby offering a promising target for intervention in clinical settings.

01 Jan 2025·Anticancer Research

Gene Expression Profiles in Ovarian Cancer Tissues as a Potential Tool to Predict Platinum-based Chemotherapy Resistance

Review

Author: Talijanovic, Melanija ; Høgdall, Estrid V ; Lopacinska-Jørgensen, Joanna

BACKGROUND/AIMOvarian cancer (OC) is one of the leading gynecological causes of death among women. The current standard treatment for OC is debulking surgery followed by platinum-based chemotherapy treatments; however, despite initial success to treatment many patients experience relapses. Currently, there are no available tests to predict sensitivity or resistance to chemotherapy. The aim of this review is to investigate the literature regarding prediction of chemotherapy resistance in patients with OC using gene expression patterns.MATERIALS AND METHODSThe literature research on PubMed resulted in a total of 490 articles published from November 20^th, 2018, to November 20^th, 2024. We selected only the original studies that described the comparison of mRNA profiles between platinum-sensitive and -resistant OC patients. Studies were included if mRNA expression was measured in human tissue by gene expression microarray, RNA sequencing and quantitative real-time PCR.RESULTSForty-four articles were included covering data from discovery cohorts obtained from hospitals and universities, as well as additional data obtained from online datasets from Gene Expression Omnibus and The Cancer Genome Atlas Program that provided either single- or multiple mRNA signatures that could discriminate between chemotherapy-sensitive and chemotherapy-resistant OC patients. OCs at all stages and histological subtypes were used but most articles included exclusively high-grade serous OC patients.CONCLUSIONmRNA-based biomarkers to predict chemotherapy resistance in patients have not yet been clinically implemented, but many differentially expressed genes between chemotherapy-resistant and -sensitive patients have been reported, such as ABCG2, DOCK4, DUSP1, DUSP4, DUSP5, GADD45B, HELQ, HOXA9, KLF4, and NR4A1, which could be compelling biomarker candidates for further studies.

01 Dec 2024·Molecular Biology Reports

The role of basic leucine zipper transcription factor E4BP4 in cancer: a review and update

Review

Author: Pan, Xinyu ; Li, Huanan ; Gu, Zhenwu ; Li, Peifen ; Wu, Yihao ; Zhang, Xueying ; Wang, Liang

Mutations in the genes of tumor cells and the disorder of immune microenvironment are the main factors of tumor development. The sensitivity of tumor cells to chemotherapy drugs affect the treatment of tumor. Nuclear transcription factor E4BP4 is dysregulated in a variety of malignant tumors. It can suppress the transcription of NFKBIA, RASSF8, SOSTDC1, FOXO-induced genes (TRAIL, FAS, GADD45a and GADD45b) and Hepcidin, up-regulate RCAN1-1 and PRNP, activate mTOR and p38 in cancer cells. Also, E4BP4 can regulate tumor immune microenvironment. TGFb1/Smad3/E4BP4/ IFNγ axis in NK cells plays an important role in antitumor immunotherapy. Over expression of E4BP4 inhibited the development of Th17 cells by directly binding to the RORγt promoter. Moreover, recent studies have shown that E4BP4 inhibited the expression of multidrug resistance genes. In this review, we summarize the molecular mechanism of E4BP4 in cancer cellular process, the effects of E4BP4 in cancer immunotherapy and antitumor drug resistance, to provide theoretical basis for tumor treatment strategies targeting E4BP4.

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GADD45B

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