GLI1
- Known as:
- GLI1
- Catalog number:
- NBP1-03294
- Product Quantity:
- 0.05 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GLI1
Related genes to: GLI1
- Gene:
- GLI1 NIH gene
- Name:
- GLI family zinc finger 1
- Previous symbol:
- GLI
- Synonyms:
- -
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-01-15
Related products to: GLI1
Related articles to: GLI1
- Fuzheng Huayu formula (FZHY) is clinically used for liver fibrosis treatment, but its pharmacological mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/05/12
Hu YonghongZhang ZhengLiang YueTang EnqiWang BibiLiu WeiMu YongpingChen GaofengLiu PingChen Jiamei - Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with poor prognosis and limited therapeutic options. Although epigenetic dysregulation is a hallmark of HCC, rational combinatorial targeting strategies remain incompletely defined. Here, we identify cooperative oncogenic functions of the chromatin modifiers enhancer of zeste homolog 2 () and lysine-specific demethylase 1 () in HCC. Analysis of the TCGA-LIHC cohort revealed that co-elevated and expressions are significantly associated with reduced overall survival. Gene set enrichment analysis demonstrated enrichment of Sonic Hedgehog (SHH) signaling and stress-responsive transcriptional programs in tumors with high expression. Functionally, dual pharmacological inhibition of (GSK126) and (SP2509) suppressed HCC cell proliferation, induced G1-phase arrest, and enhanced apoptosis, as evidenced by increased caspase-3/7 activity and decreased pro-caspase levels. Dual inhibition also impaired migration, invasion, tumor sphere formation, and stemness-associated gene expression. Mechanistically, co-targeting disrupted SHH signaling through the suppression of expression. Chromatin immunoprecipitation revealed reduced , , and occupancy at the promoter following dual inhibition, leading to the repression of and its downstream targets. Collectively, these findings demonstrate that and cooperatively sustain -dependent SHH signaling in HCC, and that dual epigenetic inhibition represents a mechanistically defined therapeutic strategy. - Source: PubMed
Publication date: 2026/04/27
Yun HongDuckGuruvaiya PonmariLevurdiak OlenaBasnakian Alexei GBoerma MarjanSafe StephenKim KyoungHyun - Medulloblastoma (MB) is the most frequent brain malignancy in children, frequently driven by deregulated Sonic Hedgehog (SHH) signaling. We previously identified the antidiabetic drug phenformin (Phen) as a potent Gli1 inhibitor that suppresses SHH-subtype MB growth. Despite its efficacy, systemic administration of Phen is limited by its potential to induce lactic acidosis, primarily through the suppression of hepatic gluconeogenesis. Here, we provide proof-of-concept that phospholipid (liposomes) and non-phospholipid (niosomes) vesicles (<200 nm) can be used to deliver phenformin selectively. Our results show that these vesicle-based delivery systems efficiently entrap Phen (around 50%) and release it into SHH MB cells, reducing proliferation and activating energy stress responses at higher doses. Furthermore, treated cells exhibit marked downregulation of SHH target genes Gli1 and Ptch1. In vivo, phenformin-loaded nanocarriers selectively increased drug accumulation in cerebellar tumors while minimizing systemic and hepatic exposure. Notably, niosomes demonstrated superior brain tumor targeting compared to free drug or liposome administration, as reflected by higher intratumoral concentrations of Phen compared to free drug or liposome administration. Consistent with this targeted delivery, we observed a substantial decline in intratumoral Gli1 and Ptch1 expression, confirming effective SHH pathway modulation. Together, these findings propose a promising nanotechnology-based method to improve phenformin therapeutic index in SHH MB by enhancing tumor specificity and reducing systemic toxicity. - Source: PubMed
Publication date: 2026/05/04
Di Magno LauraRinaldi FedericaCampea LucaDella Rocca GiorgiaForte JacopoD'Intino EleonoraCairoli SaraGoffredo Bianca MariaCarafa MariaDel Favero ElenaMarianecci CarlottaCanettieri Gianluca - Metabolic stress induced by saturated fatty acids such as palmitic acid (PA) disrupts key signalling pathways involved in neuronal survival, differentiation, and plasticity. The Sonic Hedgehog (Shh) pathway, essential for neurogenesis and tissue regeneration, is particularly vulnerable to PA-mediated suppression. In this study, we investigated the therapeutic potential of purmorphamine, a smoothened (SMO) agonist, and lithium chloride (LiCl), a GSK3β inhibitor, in restoring metabolic stress-induced insulin resistance and Shh signalling in Neuro2A cells. For the induction of insulin resistance or metabolic stress model, N2a cells were treated with PA (200 μM) for 24 h and validated by stimulation with insulin (100 nM) for various time periods 0, 5, 15, 30, 60, and 120 min. A blunted response was observed on pAKT and pGSK3β levels, indicating the development of insulin resistance. Cells were co-treated with purmorphamine (1 μM) or LiCl (10 µM) for 24 h alongside PA. PA exposure downregulated Shh components (PTCH1, SMO, Gli1) and transcriptional regulators (CREB, FOXO3), which further leads to reduced expression of neuroplasticity markers (BDNF, profilin1, SOX2) and compromised neurite outgrowth. Co-treatment with purmorphamine or LiCl significantly rescued these deficits, reinstating pathway activity and cellular function. Purmorphamine or LiCl also improved neurite outgrowth and restored the proliferative capacity of N2a cells. These findings highlight the role of GSK-3β and SMO signalling interactions in maintaining neuronal outgrowth and neuroplasticity. - Source: PubMed
Publication date: 2026/05/09
Singh PoojaAmbaliya Shonak VrujlalKumar Gajjar ShivamYadav Shreyash SantoshDatusalia Ashok Kumar - To investigate the clinicopathological and genetic characteristics of mesenchymal tumors with GLI1 gene alterations. Five cases diagnosed at the Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China from 2021 to 2025 were collected. HE and immunohistochemical slides were reviewed. Tumor-associated genetic alterations were detected using a next generation sequencing (NGS) panel of pan-solid tumor genes (468 genes, 116 DNA+352 RNA). Fluorescence in situ hybridization (FISH) was performed to detect GLI1 gene translocation and amplification. Clinical and follow-up data were analyzed. There were 3 females and 2 males, aged 48, 16, 47, 47 and 37 years, respectively. The tumor locations were the tongue, small intestine, ovary, and buttock. Histologically, tumor cells arranged in nest and lobular arrangements; within a partially myxoid stroma with necrosis and calcification, surrounded by a rich fibrovascular network around and a pseudocapsule in some cases. The tumor cells were predominantly round to oval, with fewer short spindled forms, showing mild to moderate atypia and distinct nucleoli. Immunohistochemically, tumor cells variably expressed CD56, S-100, and smooth muscle actin, but were negative for broad-spectrum epithelial markers. GLI1 immunohistochemistry showed diffuse, strong positivity (2 cases stained). Ki-67 proliferation index ranged from 1% to 30%. NGS identified PTCH1::GLI1 fusions in three cases and GLI1 amplification in two. All patients underwent complete surgical resection without adjuvant therapy. During the follow-up (4-16 months), one case recurred, while four remained disease-free. Mesenchymal neoplasm with GLI1 gene alterations is a type of tumor with low malignant potential, representing the biological behavior of low-grade sarcoma. However, it is currently not recognized by the World Health Organization classification. Surgical resection is the preferred treatment. While immunophenotyping lacks specificity, and GLI1 immunohistochemistry could aid in its diagnosis. Definitive diagnosis and differential diagnosis of this tumor require characteristic morphological features combined with molecular confirmation of GLI1 gene fusion or amplification. - Source: PubMed
Liu X GWang YLyu Y KAo Q LDuan Y Q