GLIS1

Last update 08 May 2025

Basic Info

Synonyms

FLJ36155, GLI-similar 1, GLIS family zinc finger 1

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Introduction

Acts both as a repressor and an activator of transcription (PubMed:21654807). Binds to the consensus sequence 5'-GACCACCCAC-3' (By similarity). By controlling the expression of genes involved in cell differentiation inhibits the lineage commitment of multipotent cells (PubMed:21654807). Prevents, for instance, the differentiation of multipotent mesenchymal cells into adipocyte and osteoblast (By similarity).

100 Clinical Results associated with GLIS1

100 Translational Medicine associated with GLIS1

0 Patents (Medical) associated with GLIS1

Literatures (Medical) associated with GLIS1

01 Feb 2025·eJHaem

Acute myeloid leukemia with RAM immunophenotype: A report of three patients and comprehensive literature review

Article

Author: Ghosh, Anindita ; Parisi, Xenia ; Medeiros, L. Jeffrey

AbstractIntroductionThe RAM immunophenotype (IP) in acute myeloid leukemia (AML) is defined by blasts with bright CD56 and weak‐to‐negative CD45, HLA‐DR, and CD38 expression. A RAM IP predominantly presents in infants who have “standard‐risk disease” under current criteria but, when treated accordingly, have devastatingly high rates of minimal residual disease and relapse with lower 3‐year and overall survival rates. However, given the relative rarity of this phenotype, it is neither well‐defined nor readily diagnosed.MethodsWe reviewed the electronic medical records of our institution from 1990 to 2024 for cases of AML expressing bright CD56 on flow cytometry and identified three cases with a RAM IP. Further, we performed a thorough literature search and reviewed impactful studies on pediatric AML and case/series reports of patients with a RAM IP, leading to the identification of 38 more cases.ResultsA total of 41 patients were collected. These patients were toddler age (1–3 years) with an equal sex distribution and clinically presented with low circulating blasts and cytopenias. Blasts were typically French–American–British M0 or M7. Immunophenotypically, CD33 and CD117 showed positivity in >90% of cases, with CD19, CD34, CD41, and CD42b, frequently positive. Half of the cases were positive for CD7 and CD61. T‐cell/myeloid markers were rare, except for cytoplasmic CD3, seen in 1/3, apparently correlating with CBFAT2T3:GLIS1 fusions. Gains in chromosomes 21, 13, and 8 and CBFAT2T3::GLIS1 fusions were frequent.ConclusionAML with a RAM IP has a poor prognosis. This study offers a detailed characterization of the clinicopathologic patterns associated with this rare entity, which may help formulate the most appropriate diagnostic approach.

01 Jan 2025·Life Sciences

Glis1 inhibits RTEC cellular senescence and renal fibrosis by downregulating histone lactylation in DKD

Article

Author: He, Yani ; He, Junling ; Chen, Jia ; Yang, Xin ; Bai, Lihua ; Chen, Kehong ; Wang, Xiaoyue ; Chen, Juan

BACKGROUNDAccelerated senescence of renal tubular epithelial cells (RTEC) is critical in the progression of diabetic kidney disease (DKD). GLIS family zinc finger 1 (Glis1) alleviates age-related renal fibrosis in naturally aged mice. However, the role and associated mechanism of Glis1 in accelerated senescence of RTEC and the development of DKD remain unclear.METHODSGlis1 expression was examined in the renal tubules of patients with DKD and STZ-induced DKD mice. Glis1-CKO and Glis1-overexpression mice were generated to assess the effect of Glis1 on renal dysfunction and senescence in RTEC. The interplay between Glis1 and histone lactylation during cellular senescence was elucidated in vivo and in vitro.RESULTSGlis1 expression was significantly decreased in RTEC of DKD and DKD mice. Glis1 overexpression alleviated renal dysfunction and accelerated RTEC senescence in DKD mice. Histone lactylation levels significantly increased in the kidneys of mice with DKD. Lactylation enhancers, including rotenone and nala, diminished the protective effects of Glis1 against cellular senescence, whereas treatment with sodium dichloroacetate, a lactylation inhibitor, enhanced Glis1's anti-senescence capabilities. Protein-protein interaction tools, AlphaFold2 and AutoDock, indicated that Glis1 might directly bind to the lactyltransferase KAT5 with multiple interaction sites. In vitro, the interaction between KAT5 and histone H3 was enhanced under high glucose conditions. However, Glis1 overexpression led to a significant reduction in the binding affinity between histones and KAT5, which could decrease lactylation levels.CONCLUSIONSGlis1 inhibits tubular accelerated senescence by downregulating histone lactylation and alleviating kidney fibrosis during DKD progression.

01 May 2024·Reproductive Sciences

Effect of GLIS1 on the Lymph Node Metastasis of Cervical Squamous Carcinoma Based on Transcriptome Analysis

Article

Author: Huang, Jiazhen ; Zhao, Ying

Cervical cancer remains the leading cause of cancer-related mortality among female reproductive malignancies, and lymph node metastasis (LNM) represents the major reason for its poor prognosis. In this study, we aimed to identify transcriptome differences in patients with cervical squamous cell carcinoma (CSCC) who developed LNM or not and to outline the function of GLIS1 in determining metastatic fate in CSCC. In The Cancer Genome Atlas-endocervical adenocarcinoma project, patients with LNM had shorter overall survival than those without. Transcriptome data from CSCC patients with and without LNM were analyzed to screen for differentially expressed genes (DEGs). DEGs were enriched in metastasis-related pathways, such as extracellular matrix organization, cell-cell adhesion, and regulation of tissue remodeling. GLIS1 was overexpressed in tumor tissues of patients with LNM. COMP and ITGA11 were screened as downstream targets of GLIS1. GLIS1 promoted their transcription by binding to the promoter regions of COMP and ITGA11. GLIS1 enhanced the migration, invasion, and epithelial-mesenchymal transition in CSCC cells, while the knockdown of COMP or ITGA11 reversed the promotion of GLIS1 on CSCC cell malignant phenotype. Together, our results demonstrate that GLIS1 might be related to the LNM of CSCC patients via COMP and ITGA11.

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GLIS1

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