Bulk RNA-seq of castration-resistant tumors from Ptenpc-/- mice reconstituted with either F10fl/fl or F10fl/fl; LysM-Cre+ mice

PTEN is one of the most altered tumor suppressor genes in human prostate cancer (PCa). Prostate specific-Pten-deficient mouse models develop prostate cancer eventually progressing to castration-resistant prostate cancer (CRPC), also due to alterations of the tumor immune infiltrate. By using single-cell RNA-seq, we report the identification of a subset of CD84+; CD11b+; Ly6G+; Ly6Clow immunosuppressive neutrophils that secreted the coagulation factor X (FX) into the prostate TME to directly promote PCa growth. Overall design: To characterize the impact of F10 immune cells, bulk-RNA seq was performed on Ptenpc-/- mice reconstituted with either F10fl/fl or F10fl/fl; LysM-Cre+ mice

PTEN（磷酸酶和张力蛋白同源物）是人类前列腺癌（prostate cancer, PCa）中最易发生变异的抑癌基因之一。前列腺特异性Pten敲除小鼠模型可自发形成前列腺癌，并最终进展为去势抵抗性前列腺癌（castration-resistant prostate cancer, CRPC），该进程同样与肿瘤免疫浸润的改变密切相关。本研究采用单细胞RNA测序（single-cell RNA-seq），鉴定出一类CD84+、CD11b+、Ly6G+、Ly6Clow的免疫抑制性中性粒细胞亚群，该亚群可向前列腺肿瘤微环境（tumor microenvironment, TME）中分泌凝血因子X（coagulation factor X, FX），进而直接促进前列腺癌的生长。实验整体设计：为阐明F10免疫细胞的功能效应，研究人员对分别移植了F10fl/fl或F10fl/fl; LysM-Cre+小鼠造血系统的Ptenpc-/-小鼠开展了批量RNA测序（bulk-RNA seq）