Thursday Seminar: Thomas Boyer



Thomas Boyer (PhD student, team 3)


Title: “CD52-expressing immunosuppressive myeloid cells induce mesenchymal cancer stem cells by membrane-bound TGFβ1.” Abstract: Suppressive myeloid cells play a central role in cancer escape from anti-tumor immunity. Beyond their immunosuppressive function, these cells are capable of exerting a large array of pro-tumoral activities, including the promotion of cancer cell survival, invasion and metastasis. The capability of some myeloid subsets to induce cancer stemness has recently emerged. Here we demonstrated that human immunosuppressive myeloid cells from cancer patients or generated in vitro promoted the acquisition of mesenchymal, but not epithelial, cancer stemness properties. This cancer-stemness-inducing function was restricted to only myeloid cells exerting immunosuppressive activities, and more specifically to subsets expressing the glycoprotein CD52. In mice, tumor-induced myeloid-derived immunosuppressive cells were also capable of inducing cancer stemness. Transcriptomic-, surface proteome-based interactome analyses led to the identification of membrane-bound TGFβ1 as the main mechanism of cancer stemness induction. Functional inhibition of the TGFβ1 pathway blocked the emergence of cancer stem cells induced by suppressive myeloid cells.
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