Ask about this productRelated genes to: GLCCI1 Blocking Peptide
- Gene:
- GLCCI1 NIH gene
- Name:
- glucocorticoid induced 1
- Previous symbol:
- -
- Synonyms:
- GIG18, FAM117C, TSSN1
- Chromosome:
- 7p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-06-11
- Date modifiied:
- 2016-10-05
Related products to: GLCCI1 Blocking Peptide
Related articles to: GLCCI1 Blocking Peptide
- The infiltration of regulatory T cells (Tregs) in lung adenocarcinoma (LUAD) is associated with a poor prognosis. The present study aimed to explore the potential function of Treg marker genes in prognosis and immunotherapy using the transcriptome profiles of five LUAD cohorts sourced from public databases. Among them, the single-cell dataset GSE131907 was employed to identify cell types in lung cancer tissues and to identify Treg markers. The prognostic Treg markers were screened using univariate Cox and Least Absolute Shrinkage and Selection Operator regression analyses. Subsequently, a prognostic model was constructed and assessed using Kaplan-Meier and receiver operating characteristic curves. Furthermore, the effect of prognostic Treg markers on clinical characteristics, the immune microenvironment and tumor mutation burden (TMB) were evaluated. In addition, the function of genes strongly correlated with the prognostic risk score were investigated using Spearman and functional enrichment analysis. Finally, the genes expression levels were assessed using reverse transcription-quantitative PCR (RT-qPCR) and western blotting. By analyzing the single-cell data, 13 Treg markers [centromere protein M (CENPM), pituitary tumor-transforming gene 1 protein, interleukin 1 receptor type 2, baculoviral IAP repeat containing 3, glucocorticoid induced 1 (GLCCI1), melanoma-associated antigen H1 (MAGEH1), CD5, cytokine inducible SH2 containing protein, zinc finger protein 101 (ZNF101), Ikaros family zinc finger protein 4 (IKZF4), ankyrin repeat and SOCS box protein 2, zinc finger CCCH-type containing 12D and C-C motif chemokine receptor 6] were identified as prognostic features. The prognostic model constructed using these 13 genes revealed that the high-risk group had a poorer prognosis than the low-risk group. Moreover, it was demonstrated that the risk score could be an independent prognostic factor affecting the prognosis of patients with LUAD. Additionally, the high-risk group had a lower ESTIMATE score, higher TMB score and lower T cell receptor richness than the low-risk group. Finally, RT-qPCR and western blotting showed that the expression levels of CENPM, ZNF101, MAGEH1 and IKZF4 were significantly altered in cancer tissues compared with the adjacent normal tissues. In conclusion, a reliable prognostic model based on 13 Treg markers was developed. The comprehensive characterization of the Treg markers of LUAD may help to monitor the prognosis and provide new strategies for LUAD treatment. - Source: PubMed
Publication date: 2026/04/14
He HongweiXiao ZhimingXue JijunZhang YuQu JichenWu PengHe Qiangjun - Asthma is a heterogeneous disease characterized by chronic airway inflammation and airway hyperresponsiveness. Our previous study found that glucocorticoid-induced transcript 1 (GLCCI1) is down-regulated in the lung tissues of asthmatic mice. This work attempted to determine the precise mechanism of GLCCI1 in asthma. - Source: PubMed
Publication date: 2026/01/07
Yang QingWang WeiZhu GuofengXun HanXun Qiufen - The presence of eosinophils in the lung is a decisive pathophysiological feature of asthma. Some severe asthma patients have persistent eosinophil infiltration in the lung despite receiving high-dose glucocorticoid treatment. Previous studies indicate an association between glucocorticoid-induced transcript 1 (GLCCI1) expression and the clinical efficacy of glucocorticoids. Whether there is a correlation between eosinophilic inflammation and GLCCI1 deficiency remains to be discussed. Wild-type (WT) and GLCCI1-deficient (GLCCI1) mice were sensitized with ovalbumin (OVA) to induce asthma, followed by eosinophilic inflammation assessment. CCL5 and eotaxins expression was measured in asthmatic mice and BEAS-2B bronchial epithelial cells. Mechanisms were explored using RNA-Seq, western blot, and transwell migration assays. Clinical correlations between GLCCI1 expression and CCL5 levels, eosinophil counts, or inflammatory molecules were analyzed in asthma patients' PBMCs and induced sputum. Compared to WT mice, GLCCI1 mice exhibited enhanced lung eosinophilic inflammation after OVA challenge. Both murine asthma models and BEAS-2B cell experiments revealed that GLCCI1 deficiency upregulated CCL5 expression under asthmatic conditions, potentially via the AKT pathway. Supernatant from GLCCI1-silenced BEAS-2B cells enhanced eosinophil chemotaxis, while CCL5 inhibition attenuated this effect. Clinically, GLCCI1 expression inversely correlated with blood eosinophil counts, CCL5 levels in PBMCs/sputum, and eosinophil-related molecules in asthma patients. Our findings show that GLCCI1 deficiency promotes sustained eosinophil accumulation through the upregulation of CCL5, which may be modulated by the AKT pathway. - Source: PubMed
Ge HuanJiang YuanyuanHu XinyueLuo LishaWu ChendongDeng ShuanglinziTang JialeCai RunjinGong XiaoxiaoWang GuoChen XuemeiJia YunbingLi XiaozhaoFeng Juntao - Graft-versus-host disease (GVHD) is a major complication after allogeneic hematopoietic cell transplantation (HCT), and glucocorticoids remain the standard first-line treatment. However, glucocorticoid responses vary widely and are influenced by genetic polymorphisms in glucocorticoid signaling pathways. Their impact after cord blood transplantation (CBT) is unclear. We retrospectively analyzed adult patients who underwent single-unit CBT at our institution between 2005 and 2023 with available donor or recipient DNA. Genotyping of NR3C1 (rs33388) and GLCCI1 (rs37972, rs37973) was performed using TaqMan® assays. In univariate analyses, donor GLCCI1 rs37973 AG/AA genotypes were associated with a higher incidence of grades II to IV acute GVHD but a lower incidence of chronic GVHD compared with GG donors. Multivariate analysis confirmed that GLCCI1 rs37973 AG/AA donors had a significantly reduced risk of chronic GVHD (hazard ratio 0.57, 95% confidence interval 0.35-0.93, P = 0.025). Among 30 patients who developed grades III to IV acute GVHD treated with glucocorticoids, recipient NR3C1 rs33388 TT genotype was associated with significantly lower overall survival compared with AT/AA (24.4% vs. 63.5% at 5 years, P = 0.044). These findings suggest that donor GLCCI1 rs37973 and recipient NR3C1 rs33388 polymorphisms may influence GVHD risk and survival after CBT. - Source: PubMed
Publication date: 2025/11/20
Konuma TakaakiHamatani-Asakura MegumiMonna-Oiwa MakiKato SeikoAndoh ShoheiIchimura HironaYokoyama KazuakiNannya YasuhitoTakahashi Satoshi - Allergic asthma significantly impacts individuals' quality of life and work. This study aimed to investigate the specific mechanisms by which GLCCI1 regulated mitochondrial dysfunction in allergic asthma mice. In an ovalbumin (OVA)-induced allergic asthma mouse model, mitochondrial dysfunction in airway epithelium was observed, characterized by reduced ATP production, decreased mtDNA copy number, ROS accumulation, and mitophagy activation (upregulated PINK1/OPTN). In vitro experiments confirmed that OVA stimulation impaired mitochondrial membrane potential, exacerbated oxidative stress, and reduced cell viability in bronchial epithelial cells (BECs). Moreover, GLCCI1 regulated DYRK1A/FAM117B and KEAP1/NRF2 axis while inhibiting NRF2 ubiquitination degradation. Mechanistically, GLCCI1 overexpression reversed OVA-induced mitochondrial dysfunction by activating NRF2 signaling pathway via enhancing DYRK1A/FAM117B. In allergic asthma mice, GLCCI1 overexpression improved airway hyperresponsiveness, reduced inflammatory infiltration, restored alveolar structure, and decreased IL-4/IL-5/IL-13 levels. In summary, GLCCI1 ameliorated mitochondrial dysfunction in allergic asthma mice via the DYRK1A/FAM117B/NRF2 pathway, offering a potential therapeutic target for allergic asthma. - Source: PubMed
Publication date: 2025/06/07
Xun QiufenYang QingWang WeiZhu Guofeng