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- W3094519070 abstract "In the bone marrow (BM) microenvironment, NG2 + /Nestin + mesenchymal stem cells (MSCs) promote hematopoietic stem cell (HSC) quiescence 1,2 . Importantly, the BM can also harbour disseminated tumour cells (DTCs) from multiple cancers, which, like HSCs, can remain dormant 3 . The BM signals are so growth-restrictive that dormant BM DTCs can persist for years to decades only to awaken and fuel lethal metastasis 3–10 . The mechanisms and niche components regulating DTC dormancy remain largely unknown. Here, we reveal that periarteriolar BM-resident NG2 + /Nestin + MSCs can instruct breast cancer (BC) DTCs to enter dormancy. NG2 + /Nestin + MSCs produce TGFβ2 and BMP7 and activate a quiescence pathway dependent on TGFBRIII and BMPRII, which via p38-kinase result in p27-CDK inhibitor induction. Importantly, genetic depletion of the NG2 + /Nestin + MSCs or conditional knock-out of TGFβ2 in the NG2 + /Nestin + MSCs led to awakening and bone metastatic expansion of otherwise dormant p27 + /Ki67 − DTCs. Our results provide a direct proof that HSC dormancy niches control BC DTC dormancy. Given that aged NG2 + /Nestin + MSCs can lose homeostatic control of HSC dormancy, our results suggest that aging or extrinsic factors that affect the NG2 + /Nestin + MSC niche may result in a break from dormancy and BC bone relapse." @default.
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- W3094519070 date "2020-10-22" @default.
- W3094519070 modified "2023-09-30" @default.
- W3094519070 title "NG2+/Nestin+ mesenchymal stem cells dictate DTC dormancy in the bone marrow through TGFβ2" @default.
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- W3094519070 doi "https://doi.org/10.1101/2020.10.22.349514" @default.
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