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. 2018 Feb 13;5(3):e1435180. doi: 10.1080/23723556.2018.1435180

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© 2018 The Author(s). Published with license by Taylor & Francis Group, LLC

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 1. — The pro-tumorigenic effects of oncogene-induced senescence and the senescence-associated secretory phenotype. The activation of oncogenes can lead to the onset of senescence and the activation of a Senescence-Associated Secretory Phenotype (SASP). The SASP is composed by a wide variety of factors with pleiotropic functions. Examples of common SASP factors are shown. The pro-tumorigenic activities of the SASP can be categorized as involved in 1) modulation of the immune response, 2) pro-oncogenic signaling to Cancer Stem Cells (CSCs) and/or tumor cells, 3) generating microenvironmental alterations that promote tumorigenesis. IL1A: Interleukin 1 alpha; IL1B: Interleukin 1 beta; IL6: Interleukin 6; IL8: Interleukin 8; TNF: Tumor necrosis factor; MMPs: metalloproteinases; FGFs: fibroblast growth factors; BMPs: bone morphogenetic proteins; WNTs: Wingless-related integration site proteins; EGFs: epidermal growth factor family of proteins; TGFs: transforming growth factor superfamily of proteins; EMT: epithelial-mesenchymal transition.