Fig. 1: Prostate cancer enables the establishment of a metastatic TME niche. | Nature Cell Biology

Fig. 1: Prostate cancer enables the establishment of a metastatic TME niche.

From: Prostate cancer hijacks the microenvironment

Fig. 1

Immune and non-immune components of the TME infiltrate the prostate tumour and are then primed by the tumour (for example, by uptake of tumour-derived extracellular vesicles (EVs)) to facilitate spread to metastatic sites. a, T cells infiltrate the tumour and get primed by tumour-derived EVs to express KLK3. Primed KLK3-positive T cells migrate to lymph nodes and attract PCa cells to metastasize at these sites. b, Primed non-immune cells of the TME, such as cancer-associated fibroblasts (CAFs) and activated endothelial cells (aECs), support cancer metastasis from within the tumour by modifying the extracellular matrix (ECM). c, Osteoclast (OC)-like tumour-associated macrophages (TAMs) migrate to bone and pave the way for PCa cells to metastasize at bone sites. Figure created with BioRender.com.

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