Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by beta-phenylethyl isothiocyanate.

By D. Trachootham, Yan Zhou, Hui Zhang, Y. Demizu, Zhao Chen, H. Pelicano, P. Chiao, Geetha Achanta, R. Arlinghaus, Jinsong Liu and 1 more. Cancer Cell, 2006

1,121 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4459bf69018f5a7c8476146b92f4e0b24eab8800

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Citations in the corpus

Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity (2010, background): “Previous reports indicate that cancer cells exhibit more oxidative stress than normal cells (16).”
Ferroptosis: an iron-dependent form of nonapoptotic cell death. (2012, background): “Other compounds that behave as RSLs, such as PEITC, oncrasin, and piperlongumine (Guo et al., 2008; Raj et al., 2011; Trachootham et al., 2006), trigger mitochondrial cytochrome c release, caspase activation, and other features of apoptosis not observed in cancer cells undergoing ferroptosis.”
Mitochondrial reactive oxygen species and cancer (2014, background): “In support of this model, several small molecule screens identifying compounds that specifically inhibit growth of transformed cells have converged upon glutathione utilization [110-112].”
Targeting Metabolism for Cancer Therapy (2017, background): “…that selectively kill transformed cells have identified compounds that reduce glutathione levels (Dolma et al., 2003; Raj et al., 2011; Trachootham et al., 2006), and genetic or pharmacological inhibition of glutathione synthesis results in ROS accumulation and impedes cancer…”
Redox Regulation of Cell Survival (2008, positive): “In vivo , treatment with PEITC prolonged survival of mice bearing Ras-transformed ovarian cancer (302).”
Upsides and Downsides of Reactive Oxygen Species for Cancer: The Roles of Reactive Oxygen Species in Tumorigenesis, Prevention, and Therapy (2012, neutral): “Although to our knowledge no clinical data on the efficacy and safety of PEITC with cancer patients are available, this drug has been shown to deplete cellular levels of GSH and to inhibit the activity of glutathione peroxidase (301).”
Akt determines replicative senescence and oxidative or oncogenic premature senescence and sensitizes cells to oxidative apoptosis (2008, background): “This substitution decreases the generation of ATP from glycolysis, forcing cells to increase respiration (Rossignol et al., 2004; Warburg et al., 1967).”
PGC1α Expression Defines a Subset of Human Melanoma Tumors with Increased Mitochondrial Capacity and Resistance to Oxidative Stress (2013, positive): “In fact, transformed cells have been shown to be exquisitely more sensitive to ROS-inducing drugs than nontransformed cells (Trachootham et al., 2006; Raj et al., 2011).”