A critical role for Romo1-derived ROS in cell proliferation.

Low levels of endogenous reactive oxygen species originating from NADPH oxidase have been implicated in various signaling pathways induced by growth factors and mediated by cytokines. However, the main source of is known to be the mitochondria, and increased levels of duanyu1670 from the mitochondria have been observed in many cancer cells. Thus far, the mechanism of duanyu1670 production in cancer cell proliferation in the mitochondria is not well-understood. We recently identified a novel protein, duanyu1670 modulator 1 (Romo1), and reported that increased expression of Romo1-triggered duanyu1670 production in the mitochondria. The experiments conducted in the present study showed that Romo1-derived duanyu1670 were indispensable for the proliferation of both normal and cancer cells. Furthermore, whilst cell growth was inhibited by blocking the ERK pathway in cells transfected with siRNA directed against Romo1, the cell growth was recovered by addition of exogenous hydrogen peroxide. The results of this study suggest that Romo1-induced duanyu1670 may play an important role in redox signaling in cancer cells.

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