Promotion on NLRC5 upregulating MHC-I expression by IFN-γ in MHC-I-deficient breast cancer cells.
Immunol Res
; 67(6): 497-504, 2019 12.
Article
em En
| MEDLINE
| ID: mdl-31900803
ABSTRACT
Breast cancer is the most dominant cancer in women and the second most frequent cancer in the general population worldwide. NLRC5 critically transactivates MHC class I (classically HLA-ABC in human) which is crucial for cancer immunosurveillance. But the expressional and functional impairments of NLRC5 have been found in many cancers as a major mechanism of immune evasion. Promotion of NLRC5 with the enhancement of MHC class I contributes to cancer immunotherapy and counteraction against cancer immune evasion. In many cancers, IFN-γ promotes the expression of MHC class I involving NLRC5; however, it is unclear in breast cancer cells. In this study, qRT-PCR, western blot, and flow cytometry were used to detect the mRNAs and proteins of NLRC5, ß2m, and HLA-ABC in MHC class I-deficient human SKBR3 breast cancer cells after IFN-γ treatment. It was shown that the relative levels of NLRC5 mRNA, ß2m mRNA, and HLA-ABC α heavy chain mRNA, in concentrations of 50 U/ml and 100 U/ml IFN-γ groups, were statistically increased (p < 0.05) with dose dependent tendency compared with the control group. The protein levels of NLRC5 and ß2m in concentrations of 50 U/ml and 100 U/ml IFN-γ groups, HLA-ABC (positive rates) in different concentrations of IFN-γ groups, were statistically increased (p < 0.05), with dose dependent tendency for NLRC5 and HLA-ABC, compared with the control group. Promotion of NLRC5 by IFN-γ with upregulation of MHC class I (HLA-ABC) in SKBR3 breast cancer cells, suggesting the contribution to counteracting cancer evasion from immunosurveillance and benefiting cancer immunotherapy.
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MEDLINE
Assunto principal:
Neoplasias da Mama
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Genes MHC Classe I
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Regulação para Cima
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Interferon gama
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Peptídeos e Proteínas de Sinalização Intracelular
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article