Abstract
T-lymphocyte activation plays an important role in suppressing the development of human cancers including breast cancer (BC). Cluster of differentiation 28 (CD28) is the primary T-cell costimulatory molecule and enhances T-cell activation and proliferation. To examine the role of CD28 gene polymorphism in BC, we conducted a case–control study involving 312 BC patients and 312 controls in a Chinese Han population. Bioinformatics analyses were conducted to analyze the expression level of CD28 and its association with overall survival (OS) of BC. Genotyping was performed using a custom-by-design 48-Plex single nucleotide polymorphism (SNP) Scan™ Kit. Our results indicated that CD28 mRNA level was down-regulated in the BC patients, whereas high expression of CD28 showed better OS for BC. In addition, an increased risk of BC was associated with the rs3116496 CC genotype of CD28 gene (CC vs. TT). The significant association was also observed in the recessive model. In conclusion, CD28 may be a tumor suppressor gene and rs3116496 polymorphism of CD28 gene showed positively correlation with the increased risk of BC. However, larger studies with more diverse ethnic populations are needed to confirm these results.
Highlights
Breast cancer (BC) is the most frequently diagnosed cancer among women and it is the leading cause of female cancer-related death [1]
We found that Cluster of differentiation 28 (CD28) gene expression is down-regulated in BC patients, whereas CD28 high expression is associated with better overall survival (OS) for BC by bioinformatics analysis
Tumor-specific T-cell response was beneficial to limiting the development of cancer, which was influenced by costimulatory and coinhibitory signals [17]
Summary
Breast cancer (BC) is the most frequently diagnosed cancer among women and it is the leading cause of female cancer-related death [1]. T-cell activation is dependent on the balance of costimulation and coinhibition [6]. B7 family members were identified as the coinhibitory molecular, such as cytotoxic T-lymphocyte antigen 4 (CTLA-4) and programmed cell death 1 ligand 1 (PD-L1) [8,9]. Coinhibitory molecular CTLA-4 blockade has been demonstrated to enhance antitumor immunity [11]. CD28 is encoded at the same chromosomal loci as CTLA4 and has 31% amino acid homology, and interacts closely with CTLA4 [12]. Based on these observations, CD28 was associated with the development of BC by affecting the T-cell function
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