Abstract

The clinical prognosis of breast cancer (BC) patients remains poor. Studies on BC microarrays GSE37751, GSE7390, and GSE21653 were reanalyzed to characterize the expressions of annexin A7 (ANXA7) in BC patients and the corresponding normal breast tissues and the correlation between ANXA7 expression and clinical characteristics and survivals of BC patients. Gene set enrichment analysis (GSEA) was applied to investigate the exact mechanisms as for the expression of ANXA7 and the proliferation of BC cells. The level of ANXA7 expression was significantly decreased in BC patients than that in normal controls (P < .0001). BC patients in the ANXA7 high-expression group were associated with better clinical features such as tumor size; histopathological grading; estrogen receptors; and clinical risk groups according to St Gallen criteria, Nottingham prognostic index criteria, and Veridex signature compared with those in the ANXA7 low-expression group. Higher expression of ANXA7 predicted better prognosis of BC patients.The result of GSEA indicated that ANXA7 might inhibit the proliferation of BC cells through biological processes involved in androgen response, heme metabolism, and oxidative phosphorylation. The messenger RNA and protein levels of ANXA7 were decreased in BC tissues compared with those in normal breast tissues. Our results proved that ANXA7 was downregulated in BC cells and that a higher expression of ANXA7 was associated with better prognosis of BC patients.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.