@article {1313640,
	title = {Cancer Cells Co-opt the Neuronal Redox-Sensing Channel TRPA1 to Promote Oxidative-Stress Tolerance},
	journal = {Cancer Cell},
	year = {2018},
	abstract = {Cancer cell survival is dependent on oxidative-stress defenses against reactive oxygen species (ROS) that accumulate during tumorigenesis. Here, we show a non-canonical oxidative-stress defense mechanism through TRPA1, a neuronal redox-sensing Ca2+-influx channel. In TRPA1-enriched breast and lung cancer spheroids, TRPA1 is critical for survival of inner cells that exhibit ROS accumulation. Moreover, TRPA1 promotes resistance to ROS-producing chemotherapies, and TRPA1 inhibition suppresses xenograft tumor growth and enhances chemosensitivity. TRPA1 does not affect redox status but upregulates Ca2+-dependent anti-apoptotic pathways. NRF2, an oxidant-defense transcription factor, directly controls TRPA1 expression, thus providing an orthogonal mechanism for protection against oxidative stress together with canonical ROS-neutralizing mechanisms. These findings reveal an oxidative-stress defense program involving TRPA1 that could be exploited for targeted cancer therapies.},
	url = {https://www.sciencedirect.com/science/article/pii/S1535610818301831},
	author = {Nobuaki Takahashi and Hsing-Yu Chen and Isaac Harris and Daniel Stover and Laura Selfors and Bronson, Roderick and De Raedt, Thomas and Cichowski, Karen and Yasuo Mori and Mills, Gordon and Joan Brugge}
}
