CD99 correlates with low cyclin D1, high topoisomerase 2 status and triple negative molecular phenotype but is prognostically irrelevant in breast carcinoma

Abstract

CD99 is a protein initially described in the Ewing sarcoma family of tumors, but growing evidence has shown its expression in other tumors of mesenchymal, hematopoietic and even epithelial origin. Some articles report CD99 in metaplastic carcinoma of the breast, a subtype of breast carcinoma (BC) with pronounced epithelial to mesenchymal (EMT) phenotype. Our aim was to analyse the potential relationship between CD99 and selected EMT (vimentin, E-cadherin, Twist) and proliferation markers (Ki-67, c-myc, cyclin D1, topoisomerase 2α), molecular subtypes of BC, as well as overall survival (OS) and progression-free survival (PFS). In a group of 122 cases CD99 membrane expression was seen in 14 (11.5%) cases: strong in 11 (9%) and moderate in 3 (2.5%). Expression of CD99 correlated with low cyclin D1 index, high level of topoisomerase 2α expression and lack of progesterone receptor (PR) but not with EMT characteristics. Additionally, strong expression of CD99 correlated with triple negative molecular BC phenotype. CD99 was prognostically irrelevant for OS and PFS. CD99 correlates with selected proliferative markers and low ER/PR receptor status but not with patients' outcome in BC. Further studies are required to explain precisely its role in molecular pathogenesis of BC.

Tumour cell CD99 regulates transendothelial migration via CDC42 and actin remodelling

“…Such activity is also supported by the reduced expression of CD99 mRNA in breast cancer brain metastases compared to their matched primary tumours. It has been reported that CD99 expression is not prognostic in primary breast cancer; however, CD99-expressing tumours were present in low numbers in this study ( Czapiewski et al, 2015 ). Antagonism of EGFR-mediated signalling by breast cancer CD99 ( Lee et al, 2020 ) suggests that CD99 depletion might be associated with the increased growth of metastases in our model.…”

Cyclin Y Modulates the Proliferation, Invasion, and Metastasis of Hepatocellular Carcinoma Cells

“…All the members of cyclins contain a conserved sequence that includes 100 to 150 amino acids or cyclin box that binds CDK to regulate the cell cycle and cell proliferation [ 21 ]. Previously published studies have shown that cyclin participates in a number of processes for tumor formation; cyclin A is reported to be related to the development of glioma and ovarian carcinoma [ 22 , 23 ], while cyclin D overexpression is associated with breast carcinoma and esophageal squamous cell carcinoma, and cyclin E is highly expressed in both bladder carcinoma and colorectal carcinoma [ 24 – 27 ]. Recently, a study conducted by Sun et al reported that the interaction between CCNY and serine/threonine-protein kinase PFTAIRE-1 (PFTK1) might affect HCC through a non-canonical Wnt signaling pathway [ 28 ].…”

Colony stimulating factor‑1 receptor promotes proliferation, migration and invasion in the human nasopharyngeal carcinoma 6‑10B cell line via the phosphoinositide 3‑kinase/Akt pathway

“…Furthermore, cyclin D has been widely confirmed as a biomarker in breast carcinoma (22), with its overexpression leading to tumorigenesis and malignancy. To date, cyclin D1 expression has been detected at very high levels in numerous types of malignant tumor, including head and neck squamous cell carcinoma (23), breast carcinoma (24), ovarian cancer (25), colorectal cancer (26) and gastric cancer (27).…”