索克斯10
癌症研究
埃利斯波特
黑色素瘤
小眼畸形相关转录因子
生物
免疫系统
基因敲除
转染
T细胞
免疫学
分子生物学
细胞生物学
细胞培养
转录因子
神经嵴
胚胎
生物化学
遗传学
基因
作者
Kenta Sasaki,Yoshihiko Hirohashi,Kenji Murata,Tomoyuki Minowa,Munehide Nakatsugawa,Aiko Murai,Yuka Mizue,Terufumi Kubo,Takayuki Kanaseki,Tomohide Tsukahara,Sadahiro Iwabuchi,Shinichi Hashimoto,Hisashi Uhara,Akemi Ishida‐Yamamoto,Toshihiko Torigoe
出处
期刊:Anticancer Research
[Anticancer Research USA Inc.]
日期:2023-03-27
卷期号:43 (4): 1477-1484
被引量:1
标识
DOI:10.21873/anticanres.16296
摘要
Malignant melanoma is a fatal skin cancer and is among the most immunogenic malignancies expressing melanoma-differentiation antigens and neoantigens. SRY-related HMG-box 10 (SOX10) is a transcription factor and a neural-crest differentiation marker that is used as a diagnostic marker for melanoma whilst playing a role in melanoma initiation through activation of the SOX10-MITF axis. SOX10 was shown to play a role in melanoma initiation by inducing expression of immune checkpoint molecules (e.g., HVEM and CEACAM1). In this study, we aimed to investigate the relationship between SOX10 and the expression an immune checkpoint molecule, programmed death-1 ligand 1 (PD-L1).SOX10 overexpression and knockdown was performed using SOX10 gene transfection and SOX10 siRNA transfection into A375 melanoma cells. PD-L1 expression was assessed by flow cytometry and western blotting. T cell response was evaluated using NY-ESO-1 specific TCR-transduced T (TCR-T) cells by IFNγ ELISPOT assay.SOX10 overexpression increased the expression of PD-L1, whereas SOX10 knockdown, using siRNA, decreased its expression. IFNγ ELISPOT assay revealed that overexpression of SOX10 decreased the susceptibility of cells to NY-ESO-1-specific TCR-T cells.SOX10 has a role in the intrinsic immune suppressive mechanisms of melanoma through expression of PD-L1.
科研通智能强力驱动
Strongly Powered by AbleSci AI