Inflammatory cues induce expression of immune checkpoint molecule CD137 in breast cancer cells

Authors

FRIEDLOVÁ Nela DÚCKA Monika BENEŠ Petr KNOPFOVÁ Lucia

Year of publication 2018
Type Conference abstract
Citation
Description CD137 (Tumor Necrosis Factor Receptor Superfamily, Member 9) was originally described as a T cell co-stimulatory molecule. In context of cancer it is a valuable target for immunotherapy, as the agonist CD137 antibodies induce potent T cell-mediated anti-tumor immunity. However, tumor cells utilize CD137-based strategies, such as expression of its soluble variant, in order to prevent co-stimulation of T lymphocytes. Besides, immune checkpoint molecules have been shown to promote the epithelial-mesenchymal transition, the acquisition of tumor-initiating potential and resistance to apoptosis and antitumor drugs, as well as the propensity to disseminate and metastasize. Autocrine and paracrine effects of CD137 receptor/ligand bidirectional signaling in breast cancer are still only marginally understood. We have recently described that CD137 expression is downregulated by metastasis suppressor c-Myb in mammary cancer cells. On contrary, its expression is induced by inflammatory stimuli, such as TNF?. We explore how tumor-derived CD137 affects breast cancer biology and interactions with immune/stromal cells.
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