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Fig. 7 | BMC Cancer

Fig. 7

From: Overexpression of TNFα induces senescence, autophagy and mitochondrial dysfunctions in melanoma cells

Fig. 7

Possible relationships between TNFα overexpression, apoptosis, autophagy, mitochondrial status and senescence in engineered melanoma cells A375hTNFa. Overexpression of TNFα induces weak apoptosis activation on day 1–2 and most of the cells enter survival/inflammation pathway. TNFα induces ROS production, stress and fragmentation of mitochondria. It is manifested as a mild uncoupler and causes decreased levels of intracellular ATP. Autophagy, and probably also mitophagy, are activated on day 3 and can bring mitochondrial dysfunctions too. And mitochondrial dysfunctions can be a cause of mitophagy. ALDH activity is reduced to 50% and probably cannot ensure complete detoxification of products of oxidative stress. Overexpression of TNFα induces significant overexpression of IL6, known inducer of JAK/STAT3 signalling pathway, inducer of senescence and component of SASP. Finally, autophagy, IL6, mitochondrial dysfunctions and oxidative stress caused by TNFα lead to premature senescence in malignant melanoma cells A375hTNFa. IL6 – interleukin 6, ALDH – aldehyde dehydrogenase, ROS – reactive oxygen species, SASP – senescence associated phenotype, JAK/STAT3 – signalling pathway

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