Polycomb group (PcG) complexes modify histones to silence tumor suppressor genes, which exhibit an important function in tumorigenesis and progression. The chromobox (Cbx) protein family is a critical component of PcG-mediated repression. Cbx2, a member of the Cbx protein family, is hypothesized to exhibit a vital role in breast cancer. In the present study, immunohistochemical analysis using tissue microarrays was performed to determine the levels of Cbx2 protein expression in breast cancer. The association between Cbx2 expression and the clinical features and prognosis of 455 breast cancer patients was analyzed. In addition, the efficacy of Taxol was evaluated by comparing the survival of patients with high or low Cbx2 expression. The results revealed that Cbx2 expression was higher in cancer tissues compared with adjacent normal tissues. Furthermore, high Cbx2 expression was significantly associated with large tumor size, lymph node metastasis, high TNM stage and positive human epidermal growth factor receptor-2 (HER-2) status. Patients with high Cbx2 expression also exhibited a shorter mean overall survival (OS) time (74.37 months) compared with patients with low Cbx2 expression (77.37 months). Univariate analysis indicated that high Cbx2 expression increased the risk of mortality by 1.826-fold compared with low Cbx2 expression [hazard ratio (HR), 1.826; 95% confidence interval (CI), 1.069-3.116; P=0.027]. Among patients with high Cbx2 expression, the mean OS time of individuals treated with Taxol (71.01 months) was lower compared with patients that had not received Taxol treatment (78.43 months; log-rank test statistic, 13.03; P<0.001). However, no significant difference in OS time was identified in the low expression group. The results of the current study revealed that Cbx2 may present a novel biomarker for predicting the prognosis of breast cancer patients. Cbx2 may also represent a potential target for treatment due to its important function in Taxol treatment responses.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403172PMC
http://dx.doi.org/10.3892/ol.2016.5529DOI Listing

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