ArticleScientific reports2017
Expression and Transcriptional Regulation of Human ATP6V1A Gene in Gastric Cancers.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
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- Single-Cell Transcriptomic Atlas of Chicken Ovarian Aging and Cancer Drives Prognostic Model Development.Cancers · 2026Article
- Exosome: an overview on enhanced biogenesis by small molecules.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Bioinformatics Analysis of the Expression and Prognostic Significance of Transcription Factor YY1 in Gastric Cancer.Cancer reports (Hoboken, N.J.) · 2025Article
- Micelle-Formulated Juglone Effectively Targets Pancreatic Cancer and Remodels the Tumor Microenvironment.Pharmaceutics · 2023Article
- Identification of Cancer Driver Genes by Integrating Multiomics Data with Graph Neural Networks.Metabolites · 2023Article
- Hypoxia promotes EV secretion by impairing lysosomal homeostasis in HNSCC through negative regulation of ATP6V1A by HIF-1α.Journal of extracellular vesicles · 2023Article
- High Expression of ATP6V1C2 Predicts Unfavorable Overall Survival in Patients With Colon Adenocarcinoma.Frontiers in genetics · 2022Article
- Article
- Exome-Wide Rare Variant Analysis From the DiscovEHR Study Identifies Novel Candidate Predisposition Genes for Endometrial Cancer.Frontiers in oncology · 2019Article
- Sorcin induces gastric cancer cell migration and invasion contributing to STAT3 activation.Oncotarget · 2017Article
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies demonstrate that the invasion and metastasis of gastric cancer (GC) is closely associated with a multi-subunit vacuolar H+-ATPase (V-ATPase). Here we investigated the expression and role of the human ATP6V1A gene that encodes the catalytic subunit A of V-ATPase in GC. We found that ATP6V1A expression level is significantly elevated in GCs compared to normals, but GC patients with higher expression levels of ATP6V1A have a better prognosis. Genomic analysis revealed that APT6V1A copy number is gained in a small fraction of GC patients and lost in a minimum number. Moreover, the ATP6V1A copy number was positively correlated with its mRNA level. To explore additional mechanisms by which ATP6V1A overexpressed in GCs, we investigated the relationship between transcription factor YY1 and ATP6V1A, and found that mRNA expression of YY1 had significant correlation with that of ATP6V1A. To validate that YY1 transcriptionally regulates ATP6V1A, we discovered that the ATP6V1A core promoter region contains three YY1 binding sites. Moreover, RNAi-mediated knockdown of YY1 in GC cells significantly decreased ATP6V1A mRNA and protein expression, while YY1 overexpression increased ATP6V1A expression level. In conclusion, YY1 may play an important regulatory role in ATP6V1A expression with potential mechanistic and clinical implications in GC.
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