ArticleCancer management and research2020
ATP6AP2 is Overexpressed in Breast Cancer and Promotes Breast Cancer Progression.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 6 citations in OpenAlex.
- Detection of alkaline phosphatase activity based on ATP hydrolysis and CRISPR/Cas12a.Analytical and bioanalytical chemistry · 2026Article
- Targeting the (pro)renin receptor in cancers: from signaling to pathophysiological effects.Journal of cancer research and clinical oncology · 2023Review
- Identification of immune-related features involved in Duchenne muscular dystrophy: A bidirectional transcriptome and proteome-driven analysis.Frontiers in immunology · 2022Article
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundAdenosine triphosphatase H+ transporting accessory protein 2 (ATP6AP2), also known as (pro)renin receptor, is implicated in tumorigenesis and the progression of several types of cancer. This study investigated the role of ATP6AP2 in breast cancer.
methodsUALCAN and ONCOMINE datasets were utilized to compare transcript levels of ATP6AP2 in breast cancer and normal tissues. GOBO datasets were applied to examine ATP6AP2 expression in different breast cancer cell lines. We used the cBioPortal website to explore the gene alterations and copy number alterations of ATP6AP2 in breast cancer. Cell Counting Kit-8 and transwell assays were conducted to evaluate ATP6AP2 function in MCF-7 breast cancer cells. Finally, we used the cBioPortal website to establish the interaction network of ATP6AP2 in breast cancer and performed functional enrichment analysis based on Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways.
resultsATP6AP2 was overexpressed in breast cancer tissues and breast cancer cell lines in the UALCAN, ONCOMINE, and GOBO datasets. The major type of ATP6AP2 alteration was mRNA upregulation. Moreover, ATP6AP2 was most highly expressed in luminal type breast cancer. Finally, ATP6AP2 knockdown reduced MCF-7 cell proliferation, invasion and migration. Functional enrichment analysis suggested that ATP6AP2 regulates several cancer-related pathways, especially the Wnt/β-catenin signaling pathway.
conclusionApplying multi-dimensional analytical methods, we demonstrate that ATP6AP2 is upregulated in breast cancer and may promote its development and progression.
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