作者
Sujun Chen,Guanghui Zhu,Yue Yang,Fubo Wang,Yu‐Tian Xiao,Na Zhang,Xiaojie Bian,Yasheng Zhu,Yongwei Yu,Fei Liu,Keqin Dong,Javier Mariscal,Yin Liu,Fraser Soares,Helen Loo Yau,Bo Zhang,Weidong Chen,Chao Wang,Chen Dai,Qinghua Guo,Zhengfang Yi,Mingyao Liu,Michael Fraser,Daniel D. De Carvalho,Paul C. Boutros,Dolores Di Vizio,Zhou Jiang,Theodorus H. van der Kwast,Alejandro Berlín,Song Wu,Jianhua Wang,Housheng Hansen He,Shancheng Ren
摘要
Prostate cancer shows remarkable clinical heterogeneity, which manifests in spatial and clonal genomic diversity. By contrast, the transcriptomic heterogeneity of prostate tumours is poorly understood. Here we have profiled the transcriptomes of 36,424 single cells from 13 prostate tumours and identified the epithelial cells underlying disease aggressiveness. The tumour microenvironment (TME) showed activation of multiple progression-associated transcriptomic programs. Notably, we observed promiscuous KLK3 expression and validated the ability of cancer cells in altering T-cell transcriptomes. Profiling of a primary tumour and two matched lymph nodes provided evidence that KLK3 ectopic expression is associated with micrometastases. Close cell-cell communication exists among cells. We identified an endothelial subset harbouring active communication (activated endothelial cells, aECs) with tumour cells. Together with sequencing of an additional 11 samples, we showed that aECs are enriched in castration-resistant prostate cancer and promote cancer cell invasion. Finally, we created a user-friendly web interface for users to explore the sequenced data.