Histone deacetylase 11 inhibition promotes breast cancer metastasis from lymph nodes

Patrick L. Leslie, Yvonne L. Chao, Yi-Hsuan Tsai, Subrata K. Ghosh, Alessandro Porrello, Amanda E. D. Swearingen, Emily B. Harrison, Brian C. Cooley, Joel S. Parker, Lisa A. Carey and Chad V. Pecot ()
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Patrick L. Leslie: University of North Carolina at Chapel Hill
Yvonne L. Chao: University of North Carolina at Chapel Hill
Yi-Hsuan Tsai: University of North Carolina at Chapel Hill
Subrata K. Ghosh: University of North Carolina at Chapel Hill
Alessandro Porrello: University of North Carolina at Chapel Hill
Amanda E. D. Swearingen: University of North Carolina at Chapel Hill
Emily B. Harrison: University of North Carolina at Chapel Hill
Brian C. Cooley: University of North Carolina at Chapel Hill
Joel S. Parker: University of North Carolina at Chapel Hill
Lisa A. Carey: University of North Carolina at Chapel Hill
Chad V. Pecot: University of North Carolina at Chapel Hill

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: Abstract Lymph node (LN) metastases correspond with a worse prognosis in nearly all cancers, yet the occurrence of cancer spreading from LNs remains controversial. Additionally, the mechanisms explaining how cancers survive and exit LNs are largely unknown. Here, we show that breast cancer patients frequently have LN metastases that closely resemble distant metastases. In addition, using a microsurgical model, we show how LN metastasis development and dissemination is regulated by the expression of a chromatin modifier, histone deacetylase 11 (HDAC11). Genetic and pharmacologic blockade of HDAC11 decreases LN tumor growth, yet substantially increases migration and distant metastasis formation. Collectively, we reveal a mechanism explaining how HDAC11 plasticity promotes breast cancer growth as well as dissemination from LNs and suggest caution with the use of HDAC inhibitors.

Date: 2019
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DOI: 10.1038/s41467-019-12222-5

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