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Prostate cancer cell-intrinsic interferon signaling regulates dormancy and metastatic outgrowth in bone

Title: Prostate cancer cell-intrinsic interferon signaling regulates dormancy and metastatic outgrowth in bone
Authors: Owen, KL; Gearing, LJ; Zanker, DJ; Brockwell, NK; Khoo, WH; Roden, DL; Cmero, M; Mangiola, S; Hong, MK; Spurling, AJ; McDonald, M; Chan, CL; Pasam, A; Lyons, RJ; Duivenvoorden, HM; Ryan, A; Butler, LM; Mariadason, JM; Giang Phan, T; Hayes, VM; Sandhu, S; Swarbrick, A; Corcoran, NM; Hertzog, PJ; Croucher, PI; Hovens, C; Parker, BS
Publisher Information: WILEY
Publication Year: 2020
Collection: The University of Melbourne: Digital Repository
Description: The latency associated with bone metastasis emergence in castrate-resistant prostate cancer is attributed to dormancy, a state in which cancer cells persist prior to overt lesion formation. Using single-cell transcriptomics and ex vivo profiling, we have uncovered the critical role of tumor-intrinsic immune signaling in the retention of cancer cell dormancy. We demonstrate that loss of tumor-intrinsic type I IFN occurs in proliferating prostate cancer cells in bone. This loss suppresses tumor immunogenicity and therapeutic response and promotes bone cell activation to drive cancer progression. Restoration of tumor-intrinsic IFN signaling by HDAC inhibition increased tumor cell visibility, promoted long-term antitumor immunity, and blocked cancer growth in bone. Key findings were validated in patients, including loss of tumor-intrinsic IFN signaling and immunogenicity in bone metastases compared to primary tumors. Data herein provide a rationale as to why current immunotherapeutics fail in bone-metastatic prostate cancer, and provide a new therapeutic strategy to overcome the inefficacy of immune-based therapies in solid cancers.
Document Type: article in journal/newspaper
Language: English
ISSN: 1469-221X
Relation: https://hdl.handle.net/11343/246112
Availability: https://hdl.handle.net/11343/246112
Rights: https://creativecommons.org/licenses/by-nc-nd/4.0 ; CC BY-NC-ND
Accession Number: edsbas.485CC40F
Database: BASE