| Literature DB >> 33420488 |
Sujun Chen1,2,3,4, Guanghui Zhu1,2,5,6, Yue Yang1, Fubo Wang1, Yu-Tian Xiao1, Na Zhang7, Xiaojie Bian8, Yasheng Zhu1, Yongwei Yu1, Fei Liu9, Keqin Dong1, Javier Mariscal10, Yin Liu11, Fraser Soares2, Helen Loo Yau2,3, Bo Zhang12, Weidong Chen12, Chao Wang12, Dai Chen12, Qinghua Guo12, Zhengfang Yi7, Mingyao Liu7, Michael Fraser2, Daniel D De Carvalho2,3, Paul C Boutros3,13,14,15,16,17, Dolores Di Vizio10,18,19,20, Zhou Jiang21, Theodorus van der Kwast2, Alejandro Berlin2,22, Song Wu5,6, Jianhua Wang23, Housheng Hansen He24,25, Shancheng Ren26.
Abstract
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.Entities:
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Year: 2021 PMID： 33420488 DOI： 10.1038/s41556-020-00613-6
Source DB: PubMed Journal: Nat Cell Biol ISSN： 1465-7392 Impact factor: 28.824