ATP6AP2 is Overexpressed in Breast Cancer and Promotes Breast Cancer Progression.

BACKGROUND

Adenosine 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.

METHODS

UALCAN 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.

RESULTS

ATP6AP2 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.

CONCLUSION

Applying multi-dimensional analytical methods, we demonstrate that ATP6AP2 is upregulated in breast cancer and may promote its development and progression.