Ask about this productRelated genes to: GSTM5 Blocking Peptide
- Gene:
- GSTM5 NIH gene
- Name:
- glutathione S-transferase mu 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-15
- Date modifiied:
- 2014-11-19
Related products to: GSTM5 Blocking Peptide
Related articles to: GSTM5 Blocking Peptide
- Circadian rhythm disruption has been associated with increased breast cancer risk, yet the underlying molecular drivers remain unclear. Here, we applied an integrative multi-omics framework for genetic prioritization across blood and breast tissue datasets, coupled with independent experimental validation, to systematically identify functional candidates from a pre-specified circadian rhythm-related gene set. This strategy identified glutathione S-transferase mu 5 (GSTM5) as the sole candidate gene meeting our stringent criteria, yielding robust genetic evidence suggesting a protective association against breast cancer across multiple independent datasets. In breast tumors, GSTM5 downregulation was accompanied by promoter-proximal hypermethylation, and low GSTM5 expression was associated with markers of genomic instability. In bulk cohorts, prognostic and microenvironmental associations were context-dependent and intertwined with clinicopathologic subtypes. Functionally, GSTM5 depletion impaired DNA damage repair following irradiation, and GSTM5-low breast cancer cells were preferentially sensitive to Polo-like kinase 1 (PLK1) inhibition. Collectively, these findings implicate GSTM5 deficiency in genomic instability and support further evaluation of PLK1 inhibition as a biomarker-informed therapeutic hypothesis in breast cancer. - Source: PubMed
Publication date: 2026/03/05
Ma HeLi TiankangHuang RunchengLiu YapingZhao LeiZhuang Zhigang - Migrasomes, a newly identified subtype of extracellular vesicles generated during cell migration, play crucial roles in tumor microenvironment modulation. However, their systematic characterization in lung adenocarcinoma (LUAD) remains unexplored. This study is aimed at deciphering migrasome-related molecular features and their clinical significance through multiomics integration. - Source: PubMed
Publication date: 2026/01/08
Zhou JiayuSong TianyeWang NengzhengLiang CeJiang MingZhang XuGao HongFeng Qingqing - Hyperbaric oxygen (HBO) suppresses the inflammatory response following spinal cord injury (SCI). However, the underlying detailed mechanisms are still to be clarified. Here we explored the mechanism of long non-coding RNA (lncRNA) glutathione s-transferase mu 5 (Gstm5) regulating NF-κB signaling pathway in HBO-mediated suppression of inflammatory response following SCI. In the current study, SCI cell model was developed with lipopolysaccharides (LPS)-induced BV2 cells and processed with HBO treatment, si-NC, and si-Lnc-Gstm5. Lnc-Gstm5, NF-κB p65, IL-1β，IL-6, TNF-a, suppressor of variegation 3-9 homolog 1 (SUV39H1), histone 3 lysine 9 trimethylation (H3K9me3), YTH domain containing 2 (YTHDC2) expression level were measured. The mice SCI model was generated and treated with HBO treatment, shRNA-Lnc-Gstm5. Lnc-Gstm5 was identified and BMS score, histopathological injury score, and inflammatory factors were evaluated. We found that HBO suppresses inflammatory response through up-regulating Lnc-Gstm5 level in a manner of YTHDC2-dependent m6A modification. Lnc-Gstm5 recruits SUV39H1 to up-regulate H3K9me3 expression level and suppresses NF-κB signaling pathway by reducing p65 phosphorylation. HBO suppresses the inflammatory response via YTHDC2/Lnc-Gstm5/SUV39H1/H3K9me3/NF-κB axis following SCI in mice. These results reveal a Lnc-Gstm5-driven epigenetic regulation mechanism, and targeting Lnc-Gstm5 represents a promising therapeutic strategy for SCI patients. - Source: PubMed
Publication date: 2025/12/17
Jia ShaotingLiu MoNan DingYang LuZhang JingYang JingLiu Xuehua - Bladder cancer (BCa), the most prevalent malignancy of the urinary system, is strongly associated with environmental factors including smoking and industrial chemical exposure. Although previous studies have explored the relationship between various environmental pollutants and BCa mechanisms, there is still a need for an in-depth analysis of the specific effects and particular roles of these pollutants. This study investigates the molecular mechanisms linking environmental pollutant exposure to bladder carcinogenesis through a multi-omics integrative analysis that systematically elucidates the environment-gene interaction network. By integrating transcriptomic data from multiple BCa cohorts with the Comparative Toxicogenomics Database (CTD) gene-chemical-disease network, we identified 168 environment-responsive differentially expressed genes (DEGs). Subsequent Mendelian Randomization (MR), Summary-data-based MR (SMR), and colocalization analyses revealed three causal hub genes (CTSK, GSTM5, and PAFAH1B3; PP4 > 0.70) and associated them with 34 high-risk environmental pollutants. Molecular docking demonstrated strong binding affinities between these hub genes and more than ten pollutants, with bisphenol A, sodium arsenite, and tetrachlorodibenzodioxin (TCDD) differentially regulating distinct targets: significantly suppressing tumor-suppressor genes CTSK (OR = 0.91, p = 0.004) and GSTM5 (OR = 0.77, p < 0.001) while upregulating the oncogenic factor PAFAH1B3 (OR = 2.11, p < 0.001). Single-cell RNA sequencing (scRNA-seq) analysis and Human Protein Atlas (HPA) database validation confirmed tissue-specific expression patterns of these hub genes in bladder tissues. Our findings establish a comprehensive evidence chain connecting "environmental pollutant exposure - gene interaction - bladder carcinogenesis," providing novel biomarkers and preventive targets for molecular subtyping and precision prevention of environmentally associated BCa. - Source: PubMed
Publication date: 2025/10/18
Zhu GuangqiangTan ChunlinLi Yugen - Reduced angiogenesis is a key factor in impaired healing diabetic foot ulcers. It is critical to identifying the relevant genes that regulate angiogenesis or the relevant mechanisms that accelerate angiogenesis, which is essential for the treatment of Diabetic foot ulcers (DFU). - Source: PubMed
Publication date: 2025/10/15
Huang FeiZhou YanWu HairongMa Feifei