STAT1调控MHC-I类分子在卵巢癌中的表达

Yu-Ning Fan, Chunbo He
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摘要

近年来,癌症免疫治疗取得了重大进展。然而,很少有卵巢癌患者受益于免疫治疗,预后通常很差。癌症很少被免疫细胞检测到的一个主要机制是主要组织相容性复合体I类(MHC-I)的下调,这导致细胞毒性T细胞的识别和细胞毒性降低。我们正在研究的是找到能够调节mhc - 1分子在卵巢癌中的表达的调节因子。改善MHC-I表达可能有助于患者预后良好。通过分析肿瘤转录测序数据并结合临床效果,我们确定STAT1是卵巢癌细胞中潜在的MHC-I调节因子。“湿实验室”实验证实了STAT1在MHC-I分子表达中的作用。我们的研究提示STAT1可能通过促进mhc - 1分子在卵巢癌细胞中的表达而成为促进免疫治疗应答的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
STAT1 Regulates the Expression of MHC-I Class Molecules in Ovarian Cancer
Significant advances have been made in cancer immunotherapy in recent years. However, few patients with ovarian cancer have benefited from immunotherapy and the prognosis is usually poor. A major mechanism by which cancer is rarely detected by immune cells is the downregulation of major histocompatibility complex class I (MHC-I), which leads to reduced recognition and cytotoxicity of cytotoxic T cells. What we were investigating is to find regulators that can modulate the expression of MHC-I molecules in ovarian cancer. Improving MHC-I expression may help patients to have a good prognosis. By analyzing tumoral transcriptional sequencing data and combined with clinical effects, we identified STAT1 as a potential MHC-I regulator in ovarian cancer cells. The “wet-lab” experiments confirmed the role of STAT1 in the expression of MHC-I molecules. Our study suggested that STAT1 could be a target to promote immunotherapeutic response by promoting the expression of MHC-I molecule in ovarian cancer cells.
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