Bone marrow-derived epithelial cells and hair follicle stem cells contribute to development of chronic cutaneous neoplasms

Heuijoon Park, Sonali Lad, Kelsey Boland, Kelly Johnson, Nyssa Readio, Guangchun Jin, Samuel Asfaha, Kelly S. Patterson, Ashok Singh, Xiangdong Yang, Douglas Londono, Anupama Singh, Carol Trempus, Derek Gordon, Timothy C. Wang and Rebecca J. Morris ()
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Heuijoon Park: Columbia University
Sonali Lad: University of Minnesota
Kelsey Boland: University of Minnesota
Kelly Johnson: University of Minnesota
Nyssa Readio: University of Minnesota
Guangchun Jin: Columbia University
Samuel Asfaha: Columbia University
Kelly S. Patterson: Columbia University
Ashok Singh: University of Minnesota
Xiangdong Yang: Columbia University
Douglas Londono: The State University of New Jersey
Anupama Singh: University of Minnesota
Carol Trempus: National Institute of Environmental Health Sciences
Derek Gordon: The State University of New Jersey
Timothy C. Wang: Columbia University
Rebecca J. Morris: Columbia University

Nature Communications, 2018, vol. 9, issue 1, 1-15

Abstract: Abstract We used allogeneic bone marrow transplantation (BMT) and a mouse multistage cutaneous carcinogenesis model to probe recruitment of bone marrow-derived epithelial cells (BMDECs) in skin tumors initiated with the carcinogen, dimethylbenz[a]anthracene (DMBA), and promoted with 12-O-tetradecanolyphorbol-13-acetate (TPA). BMDECs clustered in the lesional epithelium, expressed cytokeratins, proliferated, and stratified. We detected cytokeratin induction in plastic-adherent bone marrow cells (BMCs) cultured in the presence of filter-separated keratinocytes (KCs) and bone morphogenetic protein 5 (BMP5). Lineage-depleted BMCs migrated towards High Mobility Group Box 1 (HMGB1) protein and epidermal KCs in ex vivo invasion assays. Naive female mice receiving BMTs from DMBA-treated donors developed benign and malignant lesions after TPA promotion alone. We conclude that BMDECs contribute to the development of papillomas and dysplasia, demonstrating a systemic contribution to these lesions. Furthermore, carcinogen-exposed BMCs can initiate benign and malignant lesions upon tumor promotion. Ultimately, these findings may suggest targets for treatment of non-melanoma skin cancers.

Date: 2018
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DOI: 10.1038/s41467-018-07688-8

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