Human leukocyte antigen I and levels of expression of antigen-presenting element proteins plays a role in triple negative breast cancer

  • Zhu Xianglu
  • Gulizhareye Aikula
  • Mukedaisi Baiketiyaer
  • Zhang Yujing
  • Munire Mushajiang
Keywords: Triple negative breast cancer, Antigen presenting element, Human leukocyte antigen (HLA)

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)

Section
Articles

Journal Identifiers


eISSN: 1596-9827
print ISSN: 1596-5996