Ask about this productRelated genes to: GPR87 antibody
- Gene:
- GPR87 NIH gene
- Name:
- G protein-coupled receptor 87
- Previous symbol:
- GPR95
- Synonyms:
- -
- Chromosome:
- 3q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2016-10-06
Related products to: GPR87 antibody
Related articles to: GPR87 antibody
- Metastatic progression is the leading cause of mortality in lung adenocarcinoma (LUAD), yet how oncogenic signals are translated into stable metabolic and epigenetic programs that sustain tumour progression remains poorly understood. Here, through integrated single-cell, bulk, and spatial transcriptomic analyses, we identify the orphan G protein-coupled receptor GPR87 as a progression-associated regulator linked to enhanced glycolytic activity and adverse clinical outcome in LUAD. Mechanistically, GPR87 activates the cAMP/PKA/CREB pathway to induce acetyl-CoA synthetase 2 (ACSS2) transcription, thereby promoting histone H3 lysine 27 lactylation (H3K27la). H3K27la directly enhances transcription of dihydrolipoamide S-acetyltransferase (DLAT), reinforcing glycolytic flux and lactate production in a self-sustaining metabolic-epigenetic circuit. In parallel, GPR87 physically stabilizes lactate dehydrogenase A (LDHA), further amplifying lactate output. Genetic disruption of ACSS2 suppresses GPR87-driven tumour growth and metastatic colonization in vivo. Consistently, coordinated activation of this axis is enriched in advanced-stage human LUAD. Together, these findings define a GPR87-centered metabolic-epigenetic circuit that sustains glycolytic dominance and supports LUAD progression and metastasis. - Source: PubMed
Publication date: 2026/06/01
Zhang YuLi XinHan RongGuo MingyuanLin EnguangYang ChenNing JinfengZhao Yanbin - Oncolytic vaccinia virus JX-594 (pexastimogene devacirepvec) selectively replicates in tumour cells and stimulates antitumour immunity; however, its therapeutic potential in gastric cancer (GC) has not been systematically evaluated. In this study, we investigated the antitumour activity of JX-594 across a panel of 49 molecularly characterized GC cell lines and a xenograft mouse model and explored molecular features associated with viral sensitivity. JX-594 induced cytopathic effects (median effective dose, ED, 0.37 MOI (multiplicity of infection)) in a subset of gastric cancer cell lines and significantly suppressed tumour growth in vivo. Sensitivity to JX-594 varied across molecular subtypes, with microsatellite instability-high (MSI-H) cell lines showing greater susceptibility, whereas Epstein-Barr virus (EBV)-associated cell lines were relatively resistant. Transcriptomic analysis identified candidate biomarkers associated with viral sensitivity, including upregulated genes involved in G-protein signalling (GPR87, GRPR, PRDX5, MX1), interleukin production (IL1A, IL4I1), and vascular activation/dysfunction (OLR1, MMRN2), and downregulation of metastasis-related GAL3ST2. Notably, JX-594 activity was not correlated with TK1 or EGFR expression, suggesting additional determinants of viral susceptibility in GC. These findings provide preclinical evidence that molecular heterogeneity influences the response of GC to oncolytic virotherapy and support further investigation of JX-594 as a potential therapeutic strategy for gastric cancer. - Source: PubMed
Publication date: 2026/05/19
Kim Jee HungKim YeLinShin YoukeunPark InhoKwon Woo SunKim Tae SooLee NamheeOh KeunheeKim ChanJeung Hei-CheulRha Sun Young - Prior to 2024, pulmonary hypertension (PH) associated with chronic lung diseases (group 3 in the classification of PH) was subclassified according to the type of ventilatory disorder (obstructive, restrictive lung disease or mixed patterns) and not according to the lung disease itself. In 2024, the 7th World Symposium on PH proposed a revised classification, describing associations with specific lung diseases, such as COPD, interstitial lung disease and combined pulmonary fibrosis and emphysema. This update highlights the distinct pathophysiological mechanisms, clinical manifestations, outcomes and management strategies across these subgroups. Of note, a nonparenchymal restrictive lung disease subgroup has been identified, which includes patients with hypoventilation syndromes (due to kyphoscoliosis, diaphragmatic diseases, obesity hypoventilation syndrome, central hypoventilation syndromes, ) or pneumonectomy. Paradoxically, despite being one of the earliest forms of PH described, PH associated with nonparenchymal restrictive lung diseases remains among the least studied subtypes. As with all causes of group 3 PH, the primary focus of management is to address the underlying condition whenever possible. There are few data on the efficacy, safety and tolerability of the treatments approved for pulmonary arterial hypertension in this specific population. This review aims to provide updates on this condition and its management, to highlight the mechanisms of PH in each nonparenchymal restrictive lung disease and to study the relevance of the new classification and the necessary avenues of research. - Source: PubMed
Publication date: 2026/03/11
Jutant Etienne-MarieHumbert MarcMontani DavidKhoury JohadAdir Yochai - : Patients with "driver gene-negative" LUAD lack effective targeted therapies. This study aimed to elucidate the role of the glycolysis pathway in driver gene-negative LUAD to identify key genes and potential therapeutic targets. : Bulk RNA sequencing data from 49 patients with driver gene-negative LUAD were analyzed. The driver gene-negative status of patients was confirmed by immunoblotting. Gene set enrichment analysis (GSEA) was conducted on six hallmark pathways related to glycolysis. Additionally, key genes were identified and a risk score model was constructed. Finally, single-cell RNA sequencing data were processed using the Seurat package for data cleaning, dimensionality reduction clustering, and cell type identification. : GSEA analysis revealed significant enrichment of the glycolysis pathway in driver gene-negative LUAD. Differential expression analysis identified 144 genes associated with the glycolysis pathway. Six glycolysis-related genes (ANKZF1, GPR87, KIF2A, LCT, MIF, SDHC) were identified associated with poor prognosis. Single-cell sequencing analysis validated the key role of MIF in the glycolysis process and revealed a positive feedback regulatory axis between MIF and HIF-1α, which may promoting glycolysis and malignant transformation. : This study elucidated glucose metabolic reprogramming mechanisms and highlighted the MIF-HIF-1α axis as a promising therapeutic target in "driver gene-negative" LUAD, which may offer new avenues for improving outcomes, particularly those lacking conventional targeted therapy options. - Source: PubMed
Publication date: 2025/10/10
Yang Hao-ShuaiLi Yuan-HaoChen QiLuo Hong-HeYu Qi-DuoHan YuZhu WeijieZhang JinLiang Chao-Yang - Histones are the fundamental building blocks of chromatin and serve as pivotal regulators of gene expression. Differential expression and mutations of H3.1 and H3.3 genes have been implicated in the pathogenesis of various cancer types. Mutations in H3.3, especially lysine to methionine substitutions (K27M/K36M), are particularly prevalent. Moreover, genetic alterations such as G34R/W/V/L, as well as variations in and genes, have also been identified. Despite high similarity in amino acid sequences, H3.1 and H3.3 have discrete functions in cancer. In this review, we delve into the recent advances in elucidating the implications of canonical histone H3.1 and its variant H3.3 on chromatin structure and function. Additionally, we explore how potential enhancing factors such as PTEN, MLL5, GPR87 and histone chaperones influence H3.1/H3.3 function. - Source: PubMed
Publication date: 2025/09/24
Wu PengWang LiWen TingChen Qiao Yi