| Literature DB >> 25091736 |
Maria Letizia Taddei1, Lorenzo Cavallini2, Giuseppina Comito2, Elisa Giannoni2, Marco Folini3, Alberto Marini4, Paolo Gandellini3, Andrea Morandi2, Gianfranco Pintus4, Maria Rosaria Raspollini5, Nadia Zaffaroni3, Paola Chiarugi6.
Abstract
We focused our interest on senescent human-derived fibroblasts in the progression of prostate cancer. Hypoxic senescent fibroblasts promote prostate cancer aggressiveness by inducing epithelial to mesenchymal transition (EMT) and by secreting energy-rich compounds to support cancer cell growth. Hypoxic senescent fibroblasts additionally increase: i) the recruitment of monocytes and their M2-macrophage polarization, ii) the recruitment of bone marrow-derived endothelial precursor cells, facilitating their vasculogenic ability and iii) capillary morphogenesis, proliferation and invasion of human mature endothelial cells. In addition, we highlight that overexpression of the hypoxia-induced miR-210 in young fibroblasts increases their senescence-associated features and converts them into cancer associated fibroblast (CAF)-like cells, able to promote cancer cells EMT, to support angiogenesis and to recruit endothelial precursor cells and monocytes/macrophages.Entities:
Keywords: Prostate cancer; Senescence; Tumor microenvironment; miR-210
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Year: 2014 PMID: 25091736 PMCID: PMC5528604 DOI: 10.1016/j.molonc.2014.07.009
Source DB: PubMed Journal: Mol Oncol ISSN: 1574-7891 Impact factor: 6.603