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학술저널
저자정보
송인혜 (서울아산병원) 김영애 (NeogenTC Corp. Seoul) 허선희 (서울아산병원 병리과) 방원선 (서울아산병원) 박혜선 (주식회사 네오젠티씨) 최연호 (NeogenTC Corp. Seoul) 이희재 (주식회사 네오젠티씨) 서정한 (주식회사 네오젠티씨) 조영진 (울산대학교) 정성욱 (울산대학교) 김희정 (울산대학교) 안세현 (서울아산병원) 이희진 (서울아산병원) 공경엽 (서울아산병원)
저널정보
대한암학회 Cancer Research and Treatment Cancer Research and Treatment 제54권 제4호
발행연도
2022.10
수록면
1,111 - 1,120 (10page)
DOI
10.4143/crt.2021.1017

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PurposeThe expression of major histocompatibility complex class I (MHC I) has previously been reported to be negatively associated with estrogen receptor (ER) expression. Furthermore, MHC I expression, level of tumor-infiltrating lymphocytes (TILs), and expression of interferon (IFN) mediator MxA are positively associated with one another in human breast cancers. This study aimed to investigate the mechanisms of association of MHC I with ER and IFN signaling.Materials and MethodsThe human leukocyte antigen (HLA)-ABC protein expression was analyzed in breast cancer cell lines. The expressions of <i>HLA</i>-<i>A</i> and <i>MxA</i> mRNAs were analyzed in MCF-7 cells in Gene Expression Omnibus (GEO) data. ER and HLA-ABC expressions, Ki-67 labeling index and TIL levels in tumor tissue were also analyzed in ER+/ human epidermal growth factor receptor 2 (HER2)- breast cancer patients who randomly received either neoadjuvant chemotherapy or estrogen modulator treatment followed by resection.ResultsHLA-ABC protein expression was decreased after β-estradiol treatment or hESR-GFP transfection and increased after fulvestrant or IFN-γ treatment in cell lines. In GEO data, <i>HLA</i>-<i>A</i> and <i>MxA</i> expression was increased after ESR1 shRNA transfection. In patients, ER Allred score was significantly lower and the HLA-ABC expression, TIL levels, and Ki-67 were significantly higher in the estrogen modulator treated group than the chemotherapy treated group.ConclusionMHC I expression and TIL levels might be affected by ER pathway modulation and IFN treatment. Further studies elucidating the mechanism of MHC I regulation could suggest a way to boost TIL influx in cancer in a clinical setting.

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