Expression of STAT1 is positively correlated with PD-L1 in human ovarian cancer
Expression of STAT1 is positively correlated with PD-L1 in human ovarian cancer
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人卵巢癌中STAT1的表达与PD-L1呈正相关
DOI：
10.1080/15384047.2020.1824479
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发表时间：
2020-10-11
影响因子：
3.6
通讯作者：
Xu, Guoxiong
中科院分区：
文献类型：
--
作者：
Liu, Fangran;Liu, Jiao;Xu, Guoxiong
信号转导子和转录激活子1（STAT1）与肿瘤发生的免疫微环境有关。程序性细胞死亡1（PD-1）及其配体（PD-L1）通过介导肿瘤免疫逃逸而在免疫治疗中发挥重要作用。阻断PD-1/PD-L1通路可以恢复内源性抗肿瘤免疫应答。本研究旨在检测STAT1、PD-1和PD-L1的表达以及人类上皮性卵巢癌（EOC）中选定标志物之间的相关性。结果显示，恶性肿瘤中STAT1、PD-1和PD-L1阳性细胞较多。在卵巢肿瘤患者中，STAT1和PD-L1的表达与年龄相关，而PD-1和PD-L1与组织病理学类型相关。STAT1的表达与浆液性癌的临床分期和分级有关。STAT1在OC细胞中的表达高于正常卵巢表面上皮细胞，且与PD-L1表达呈正相关。STAT 1的敲低降低了PD-L1的表达，而STAT 1的过表达增加了PD-L1的表达。此外，STAT1、PD-1和PD-L1在紫杉醇耐药细胞中的表达低于敏感细胞。最后，STAT1影响EOC患者的总生存期和无进展生存期。这些发现表明STAT1、PD-1和PD-L1是EOC的组织标志物，并暗示高水平的STAT1、PD-1和PD-L1可能有利于EOC患者的检查点免疫治疗，但由于STAT1、PD-1和PD-L1在紫杉醇耐药细胞中的低表达，可能在紫杉醇耐药患者中具有限制。
Signal transducer and activator of transcription 1 (STAT1) is related to the immunemicroenvironmentof tumorigenesis. The programmed cell death 1 (PD-1) and its ligand (PD-L1) have been reported to be important in immunotherapy by mediating tumor immune evasion. Blocking the PD-1/PD-L1 pathway can restore the endogenous anti-tumor immune response. This study aimed to examine the expression of STAT1, PD-1, and PD-L1 and the correlation between selected markers in human epithelial ovarian cancer (EOC). The results showed that malignant tumors contained more STAT1, PD-1, and PD-L1 positive cells. The expression of STAT1 and PD-L1 was associated with age, whereas PD-1 and PD-L1 associated with histopathological type, in patients with ovarian tumors. Moreover, the expression of STAT1 was found to be associated with disease stages and the grade of serous carcinoma. STAT1 expression was higher in OC cells than normal ovarian surface epithelial cells and was positively correlated with PD-L1 expression. The knockdown of STAT1 decreased PD-L1 expression, whereas overexpression of STAT1 increased PD-L1 expression. Furthermore, the expression of STAT1, PD-1, and PD-L1 was lower in paclitaxel-resistant cells than sensitive cells. Finally, STAT1 affected the overall survival and progression-free survival of patients with EOC. These findings suggest that STAT1, PD-1, and PD-L1 are the tissue markers of EOC and imply the possibility that the high level of STAT1, PD-1, and PD-L1 may favor the checkpoint immunotherapy in patients with EOC, but may have a limit in paclitaxel-resistant patients because of the low expression of STAT1, PD-1, and PD-L1 in paclitaxel-resistant cells.