Monocytic and granulocytic myeloid derived suppressor cells differentially regulate spatiotemporal tumour plasticity during metastatic cascade

Maria Ouzounova, Eunmi Lee, Raziye Piranlioglu, Abdeljabar El Andaloussi, Ravindra Kolhe, Mehmet F. Demirci, Daniela Marasco, Iskander Asm, Ahmed Chadli, Khaled A. Hassan, Muthusamy Thangaraju, Gang Zhou, Ali S. Arbab, John K. Cowell and Hasan Korkaya ()
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Maria Ouzounova: Georgia Cancer Center, Augusta University
Eunmi Lee: Georgia Cancer Center, Augusta University
Raziye Piranlioglu: Georgia Cancer Center, Augusta University
Abdeljabar El Andaloussi: Georgia Cancer Center, Augusta University
Ravindra Kolhe: Georgia Cancer Center, Augusta University
Mehmet F. Demirci: Georgia Cancer Center, Augusta University
Daniela Marasco: University of Naples Federico II
Iskander Asm: Georgia Cancer Center, Augusta University
Ahmed Chadli: Georgia Cancer Center, Augusta University
Khaled A. Hassan: Comprehensive Cancer Center, University of Michigan
Muthusamy Thangaraju: Georgia Cancer Center, Augusta University
Gang Zhou: Georgia Cancer Center, Augusta University
Ali S. Arbab: Georgia Cancer Center, Augusta University
John K. Cowell: Georgia Cancer Center, Augusta University
Hasan Korkaya: Georgia Cancer Center, Augusta University

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract It is widely accepted that dynamic and reversible tumour cell plasticity is required for metastasis, however, in vivo steps and molecular mechanisms are poorly elucidated. We demonstrate here that monocytic (mMDSC) and granulocytic (gMDSC) subsets of myeloid-derived suppressor cells infiltrate in the primary tumour and distant organs with different time kinetics and regulate spatiotemporal tumour plasticity. Using co-culture experiments and mouse transcriptome analyses in syngeneic mouse models, we provide evidence that tumour-infiltrated mMDSCs facilitate tumour cell dissemination from the primary site by inducing EMT/CSC phenotype. In contrast, pulmonary gMDSC infiltrates support the metastatic growth by reverting EMT/CSC phenotype and promoting tumour cell proliferation. Furthermore, lung-derived gMDSCs isolated from tumour-bearing animals enhance metastatic growth of already disseminated tumour cells. MDSC-induced ‘metastatic gene signature’ derived from murine syngeneic model predicts poor patient survival in the majority of human solid tumours. Thus spatiotemporal MDSC infiltration may have clinical implications in tumour progression.

Date: 2017
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DOI: 10.1038/ncomms14979

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