Expression levels of ABCG2 and CD61 genes in breast cancer tissues of Iranian population.

ABSTRACT

Breast cancer as the most common female cancer is a malignancy with heterogeneous course. Dysregulation of several genes has been associated with development of this malignancy. Among these genes are the stem cell markers CD61 and breast cancer resistance protein (BCRP or ATP-binding cassette super-family G member 2 (ABCG2)). ABCG2 is one of the major efflux transporters implicated in multidrug resistance in cancer cells. In the present study, we compared expression of CD61 and ABCG2 transcripts between 30 breast cancer tissues and matched adjacent non-cancerous tissues (ANCTs) using real time qPCR technique. There was no significant difference in expression of CD61 or ABCG2 between tumoral tissues and ANCTs (Expression ratios = 1.21 and 0.98, P values = 0.55 and 0.96, respectively). There was a trend toward association between relative expression of CD61 (tumoral tissues versus ANCTs) and patients' age (P = 0.05) in a way that older patients tended to over-express this marker in their tumoral tissues compared with the matched ANCTs. Moreover, there was a significant association between expression of this gene and tumor size (P = 0.04) in a way that all tumors with sizes less than 2 cm showed down-regulation of CD61 (as compared with the matched ANCTs). Expression of CD61 was significantly higher in tumor tissues with extracapsular nodal extension compared with confined lesions (P = 0.007). Moreover, expression of ABCG2 was significantly higher in tumor tissues of patients aged less than 55 years compared with older patients (P = 0.04). There was no significant correlation between expression of CD61 and ABCG2 either in tumoral tissues or in ANCTs. The current investigation shows association or trends toward association between expression of two cancer stem cell markers and some clinical data of breast cancer patients such as extracapsular nodal extension, age and tumor size which might imply their importance in the pathogenesis of breast cancer.