Calpain system protein expression in basal-like and triple-negative invasive breast cancer

Storr, Sarah J.; Lee, K.W.; Woolston, Caroline M.; Safuan, Sabreena; Green, A.R.; Macmillan, R.D.; Benhasouna, A.; Parr, T.; Ellis, I.O.; Martin, Stewart G.

Abstract

Background: Basal-like and triple-negative breast tumours encompass an important clinical subgroup and
biomarkers that can prognostically stratify these patients are required.
Materials and methods: We investigated two breast cancer tissue microarrays for the expression of calpain-1,
calpain-2 and calpastatin using immunohistochemistry. The first microarray was comprised of invasive tumours from
1371 unselected patients, and the verification microarray was comprised of invasive tumours from 387 oestrogen
receptor (ER)-negative patients.
Results: The calpain system contains a number of proteases and an endogenous inhibitor, calpastatin. Calpain activity
is implicated in important cellular processes including cytoskeletal remodelling, apoptosis and survival. Our results show
that the expression of calpastatin and calpain-1 are significantly associated with various clinicopathological criteria
including tumour grade and ER expression. High expression of calpain-2 in basal-like or triple-negative disease was
associated with adverse breast cancer-specific survival (P = 0.003 and

• Journal Article Type: Article
• Publication Date: Sep 9, 2012
• Journal: Annals of Oncology
• Print ISSN: 0923-7534
• Electronic ISSN: 0923-7534
• Publisher: Oxford University Press
• Peer Reviewed: Peer Reviewed
• Volume: 23
• Issue: 9
• APA6 Citation: Storr, S. J., Lee, K., Woolston, C. M., Safuan, S., Green, A., Macmillan, R., …Martin, S. G. (2012). Calpain system protein expression in basal-like and triple-negative invasive breast cancer. Annals of Oncology, 23(9), doi:10.1093/annonc/mds176
• DOI: https://doi.org/10.1093/annonc/mds176
• Publisher URL: http://annonc.oxfordjournals.org/content/23/9/2289.full
• Copyright Statement: Copyright information regarding this work can be found at the following address: http://creativecommons.org/licenses/by-nc/4.0