Convergent alterations in the tumor microenvironment of MYC-driven human and murine prostate cancer

Mindy K. Graham, Rulin Wang, Roshan Chikarmane, Bulouere Abel, Ajay Vaghasia, Anuj Gupta, Qizhi Zheng, Jessica Hicks, Polina Sysa-Shah, Xin Pan, Nicole Castagna, Jianyong Liu, Jennifer Meyers, Alyza Skaist, Yan Zhang, Michael Rubenstein, Kornel Schuebel, Brian W. Simons, Charles J. Bieberich, William G. Nelson, Shawn E. Lupold, Theodore L. DeWeese, Angelo M. De Marzo and Srinivasan Yegnasubramanian ()
Additional contact information
Mindy K. Graham: School of Medicine
Rulin Wang: School of Medicine
Roshan Chikarmane: School of Medicine
Bulouere Abel: School of Medicine
Ajay Vaghasia: School of Medicine
Anuj Gupta: School of Medicine
Qizhi Zheng: School of Medicine
Jessica Hicks: School of Medicine
Polina Sysa-Shah: School of Medicine
Xin Pan: School of Medicine
Nicole Castagna: School of Medicine
Jianyong Liu: School of Medicine
Jennifer Meyers: School of Medicine
Alyza Skaist: School of Medicine
Yan Zhang: School of Medicine
Michael Rubenstein: University of Maryland at Baltimore County
Kornel Schuebel: School of Medicine
Brian W. Simons: Baylor College of Medicine
Charles J. Bieberich: University of Maryland at Baltimore County
William G. Nelson: School of Medicine
Shawn E. Lupold: School of Medicine
Theodore L. DeWeese: School of Medicine
Angelo M. De Marzo: School of Medicine
Srinivasan Yegnasubramanian: School of Medicine

Nature Communications, 2024, vol. 15, issue 1, 1-20

Abstract: Abstract How prostate cancer cells and their precursors mediate changes in the tumor microenvironment (TME) to drive prostate cancer progression is unclear, in part due to the inability to longitudinally study the disease evolution in human tissues. To overcome this limitation, we perform extensive single-cell RNA-sequencing (scRNA-seq) and molecular pathology of the comparative biology between human prostate cancer and key stages in the disease evolution of a genetically engineered mouse model (GEMM) of prostate cancer. Our studies of human tissues reveal that cancer cell-intrinsic activation of MYC signaling is a common denominator across the well-known molecular and pathological heterogeneity of human prostate cancer. Cell communication network and pathway analyses in GEMMs show that MYC oncogene-expressing neoplastic cells, directly and indirectly, reprogram the TME during carcinogenesis, leading to a convergence of cell state alterations in neighboring epithelial, immune, and fibroblast cell types that parallel key findings in human prostate cancer.

Date: 2024
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DOI: 10.1038/s41467-024-51450-2

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