Abstract
Purpose : To determine the protein expression levels of leukocyte antigen I and antigen-presenting element (APM) genes, and to study their relationship with triple negative breast cancer (TNBC) in patients from Uyghur and Han, China. Methods : Immunohistochemistry was used to determine the expression levels of 10 proteins (HLA-A (Human Leukocyte Antigens-A), HLA-B, HLA-C, TAP1 (Transporter associated with Antigen Processing-1), TAP2, calreticulin, calnexin, ERp57 (Endoplasmic reticulum resident protein 57), ERAP1 (Type 1 tumor necrosis factor receptor shedding aminopeptidase regulator) and tapasin) in TNBC and non-TNBC tissue specimens, and 26 benign lesions (fibrous adenoma) specimens from 120 Uygur and Han women. Results : Immunohistochemical analysis showed that the positive expressions of HLA-A, HLA-B, TAP2, Erp57, ERAP1, calnexin and calreticulin in breast cancer tissues were significantly lower than those in breast fibroma tissues (p < 0.05). Among the 86 TNBC patients, there were 35 cases of tapasin- (40.70 %), 26 cases of tapasin+ (30.30 %), and 25 cases of tapasin++ (29.10 %). Among the 34 non-TNBC patients, there were 25 cases of tapsin- (73.50 %), 7 cases of tapasin+ (20.60 %) and 2 cases of tapasin ++ (5.9 %). The positive expression of tapasin in TNBC patients was significantly higher than that in non-TNBC patients (p < 0.05). Conclusion : Down-regulation of transcriptional expression or loss of protein expression of HLA-I and APM genes is closely related to the progression of breast cancer, and is therefore, a potential molecular marker for screening tumors. Keywords : Triple negative breast cancer, Antigen presenting element, Human leukocyte antigen (HLA)
Highlights
Triple negative breast cancer, a subtype of breast cancer, refers to breast cancer that does not express PR, ER and HER-2
Tumor tissue samples (120) were taken from Uyghur women and Han women with triple negative breast cancer (TNBC) and non-TNBC by operation, and 26 samples of benign lesion tissues were taken from patients with fibroadenoma, one of which was used for pathological immunohistochemical identification and the other was immediately frozen in liquid nitrogen and stored in an ultra-low temperature freezer at -80 °C
Results from immunohistochemistry revealed that the positive expressions of Human leukocyte antigen (HLA)-A, HLA-B, TAP2, calnexin, calreticulin, Erp57 and ERAP1 were much lower in breast cancer tissues that those in breast fibroadenoma tissues, while there were no significant differences in the expressions of HLAC, TAP1 and tapasin between benign tissues and breast cancer tissue. These results suggest that the expressions of antigen-presenting element (APM) family of genes in breast cancer cells is out of control, a situation which may hinder the correct assembling and loading of HLA-I molecules after transcription, and the presentation of endogenous antigenic peptides
Summary
A subtype of breast cancer, refers to breast cancer that does not express PR, ER and HER-2. Tumor cells usually generate tumor-related antigens, and the immune system can recognize, monitor and eliminate these antigens [1]. When the antigen presenting function is defective or fails, and when tumor cells get the ability to overwhelm the. As an important surface marker in cells, HLA is closely related to malignant cancer and it plays an essential role in immune regulation and immune response. The structure and function of APM are very important in the process of endogenous antigen peptide presentation in vivo. When its structure and function are impaired, tumor cells can get rid of the surveillance by the immune system [3]. The present study was carried out to determine the protein expression levels of HLA-I and APM in cancer tissue samples from Uyghur and Han TNBC patients, and to investigate the relationship between these proteins and TNBC
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
