Journal
GENOME RESEARCH
Volume 28, Issue 5, Pages 625-638Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gr.229070.117
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Funding
- Cancer Australia [1044458]
- National Health and Medical Research Council [535903, 1070418, 1106870, 1063559, 1002648, 1102752, 1035721, 1058540]
- Cancer Institute of New South Wales Fellowship [14/ECF/1-23]
- Australian Prostate Cancer Research Centre-NSW
- Prostate Cancer Foundation of Australia (Movember Young Investigator Grant) [YI0911]
- Victorian Cancer Agency
- RT Hall Trust
- TissuPath Pathology
- National Health and Medical Research Council of Australia [1102752, 1106870, 1070418, 1058540] Funding Source: NHMRC
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The growth and progression of solid tumors involves dynamic cross-talk between cancer epithelium and the surrounding microenvironment. To date, molecular profiling has largely been restricted to the epithelial component of tumors; therefore, features underpinning the persistent protumorigenic phenotype of the tumor microenvironment are unknown. Using whole-genome bisulfite sequencing, we show for the first time that cancer-associated fibroblasts (CAFs) from localized prostate cancer display remarkably distinct and enduring genome-wide changes in DNA methylation, significantly at enhancers and promoters, compared to nonmalignant prostate fibroblasts (NPFs). Differentially methylated regions associated with changes in gene expression have cancer-related functions and accurately distinguish CAFs from NPFs. Remarkably, a subset of changes is shared with prostate cancer epithelial cells, revealing the new concept of tumor-specific epigenome modifications in the tumor and its microenvironment. The distinct methylome of CAFs provides a novel epigenetic hallmark of the cancer microenvironment and promises new biomarkers to improve interpretation of diagnostic samples.
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