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Non-autonomous Tumor Progression by Oncogenic Inflammation

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Chronic Inflammation
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Abstract

Defects in Mitochondrial respiratory function is frequently observed in human cancers. However, the mechanism by which mitochondrial dysfunction contributes to tumour growth and progression has been unclear. Recent studies in Drosophila epithelium have uncovered that mitochondrial defects induce tumour progression of surrounding tissue by cooperating with oncogenic Ras. Simultaneous Ras activation and mitochondrial dysfunction cause chronic ‘oncogenic inflammation’, which induces overgrowth and metastatic behavior in neighbouring benign tumours via upregulation of an IL-6-like inflammatory cytokine Upd. Further genetic analyses revealed that the nonautonomous tumour progression by oncogenic inflammation is caused through cellular senescence and senescence-associated secretary phenotype (SASP). These findings provide a novel mechanistic basis for tumour progression through cell–cell communication triggered by Ras activation and mitochondrial dysfunction, frequent alterations in human cancers.

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Correspondence to Tatsushi Igaki .

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Ohsawa, S., Igaki, T. (2016). Non-autonomous Tumor Progression by Oncogenic Inflammation. In: Miyasaka, M., Takatsu, K. (eds) Chronic Inflammation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-56068-5_17

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