Ask about this productRelated genes to: VSIG1 antibody
- Gene:
- VSIG1 NIH gene
- Name:
- V-set and immunoglobulin domain containing 1
- Previous symbol:
- -
- Synonyms:
- MGC44287, GPA34
- Chromosome:
- Xq22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-02
- Date modifiied:
- 2019-03-21
Related products to: VSIG1 antibody
Related articles to: VSIG1 antibody
- To establish a doxorubicin (DOX)-resistant acute myeloid leukemia (AML) cell line and explore the mechanisms of its drug resistance. - Source: PubMed
Feng Lu-LuWang Yu-TingHuang Chao-FanSun Cong-YongJun Ya-LiZhang Li - Hepatocellular carcinoma (HCC) is a heterogeneous primary liver malignancy characterized by limited treatment options and low overall survival rates. Recent studies have explored the role of programmed death ligand 1 (PD-L1), tumor-associated macrophages (TAMs), and epithelial-mesenchymal transition (EMT) in modulating tumor progression and the response to immunotherapy. This study aimed to investigate the association among PD-L1 expression, TAMs, and EMT in HCC, highlighting the recently proposed immunophenotypic variant-gastric-type HCCs. A retrospective cohort of 50 surgically resected HCC patients was analyzed. Immunohistochemical staining was performed for PD-L1 (clones 28-8 and 22C3), CD68 (TAMs), and EMT markers (VSIG-1, TTF-1, and vimentin). PD-L1 expression was detected in 52% of the patients and was significantly associated with high TAM counts ( < 0.001). Compared with PD-L1-negative patients, those with gastric-type HCCs, which are characterized by VSIG-1 and TTF-1 co-expression and vimentin negativity, demonstrated improved survival outcomes ( = 0.03). Integration of immune and EMT profiling of tumor cells in routine diagnostics may guide prognosis and immunotherapeutic strategies in HCC. Further molecular validation is required to confirm the biological significance of the proposed gastric-type HCC immunophenotype. - Source: PubMed
Publication date: 2026/07/06
Szodorai RitaKovalszky IlonaDezső KatalinGurzu Simona - V-set and immunoglobulin domain-containing 1 (VSIG1) is a member of the immunoglobulin superfamily that has attracted increasing attention as a differentiation-associated protein in gastrointestinal neoplasia. Although initially described as a gastric-specific marker, accumulating evidence indicates that VSIG1 more accurately reflects gastric-enriched epithelial differentiation rather than strict anatomical origin. This conceptual shift has implications for phenotype-oriented tumor classification and diagnostic interpretation in the context of lineage plasticity. A structured and transparently reported literature search was conducted in PubMed/MEDLINE, Web of Science, and Scopus, covering studies published between 2000 and 2024. Eligible studies included original research and relevant reviews evaluating VSIG1 expression in normal tissues and digestive tract tumors, with emphasis on immunohistochemical patterns and clinicopathological correlations. In gastric cancer, VSIG1 expression consistently correlates with preserved glandular architecture and epithelial differentiation, whereas reduced or absent expression accompanies dedifferentiation and architectural disorganization. Outside the stomach, VSIG1 positivity is uncommon but reproducible in tumors exhibiting gastric-type or mixed differentiation, including settings of hepato-gastric phenotypic overlap. These patterns support interpretation of VSIG1 as a context-dependent indicator of lineage engagement and differentiation state rather than tumor origin or aggressiveness. Current data on independent prognostic value are limited and partially conflicting, and predictive roles remain unsupported, while functional data remain limited. - Source: PubMed
Publication date: 2026/03/08
Satala Catalin-BogdanPatrichi GabrielaGurau Alina-MihaelaOnofrei Popa AndreeaMihalache Daniela - Tetraodontiformes species exhibit several evolutionary innovations, notably the convergent evolution of two traits in some clades: defensive body inflation and the loss of acid-peptic digestion. It has been widely believed that the evolution of body inflation drove the loss of gastric digestion, as ingesting seawater during inflation would hinder acidification and ultimately lead to the loss of gastric digestion. Leveraging accumulating genome resources, we investigated the presence, synteny, gene expression, and rapid evolution of nine genes associated with acid-peptic digestion across seven species from four Tetraodontiformes families, representing two branches that underwent convergent evolution. In the first evolutionary branch, all agastric species-including the species lacking inflation capability (Mola mola)-exhibit loss or pseudogenization of eight gastric-function-related genes. Among these, only pga1 is retained, though it lacks digestive functionality. In another branch, the greenfin horse-faced filefish (Thamnaconus septentrionalis), which possesses a functional stomach, maintains solely pga2 as its single pepsinogen gene, with pga1 and pgc having been lost, while slc26a9 and vsig1 show evidence of rapid evolution. These findings suggest that the convergent loss of gastric digestion likely occurred before the evolution of body inflation in both branches, supporting an "unfunctional-stomach-first" evolutionary scenario. - Source: PubMed
Publication date: 2025/07/01
Liu ChangLin LeiDu ShengLiu KaiqiangJi HonglongWang QianHe YangbinShao Changwei - The stomach has been a highly conserved organ throughout vertebrate evolution; however, there are now over 20 lineages composed of monotremes, lungfish and teleost fish displaying a secondary loss of stomach function and morphology. This "agastric phenotype" has evolved convergently and is typified by a loss of gastric glands and gastric acid secretion and a near-to-complete loss of storage capacity of the stomach. All agastric species have lost the genes for gastric enzymes ( and ) and proton pump subunits ( and ), and gastrin () has been lost in monotremes. As a key gastric hormone, the conservation of gastrin has not yet been investigated in the lungfish or agastric teleosts, and it is unclear how the loss of gastrin affects the evolution and selection of the native receptor (), gastrin-releasing peptide () and gastrin-releasing peptide receptor () in vertebrates. Furthermore, there are still many genes implicated in gastric development and function which have yet to be associated with the agastric phenotype. We analysed the evolution, selection and conservation of the gastrin pathway and a novel gastric gene repertoire (, , , , and ) to determine the correlation with the agastric phenotype. We found that the loss of gastrin or its associated genes does not correlate with the agastric phenotype, and their conservation is due to multiple pleiotropic roles throughout vertebrate evolution. We found a loss of the gastric gene repertoire in the agastric phenotype, except in the echidna, which retained several genes (, and ). Our findings suggest that the gastrin physiological pathway evolved differently in pleiotropic roles throughout vertebrate evolution and support the convergent evolution of the agastric phenotype through shared independent gene-loss events. - Source: PubMed
Publication date: 2025/08/05
Dann JacksonGrützner Frank