%0 Journal Article %T Activation of c-Met in cancer cells mediates growth-promoting signals against oxidative stress through Nrf2-HO-1 %A David Zurakowski %A Evelyn Flynn %A Murugabaskar Balan %A Samik Chakraborty %A Soumitro Pal %A Toni K. Choueiri %J Archive of "Oncogenesis". %D 2019 %R 10.1038/s41389-018-0116-9 %X c-Met induction protects the renal cancer cells from sorafenib-induced ROS generation, DNA damage, and apoptosis. a¨Cf 786-O cells were subjected to combination treatments with HGF (50£¿ng/ml), sorafenib (10£¿¦ÌM) or only vehicle for 24£¿h. a Apoptotic cell deaths were measured by annexin V (APC) and propidium iodide staining through flow cytometry. b Cell proliferation was measured by MTT assay. c Following treatment, cells were stained by using oxidative stress detection reagent and checked for endogenous reactive oxygen species (ROS) through flow cytometry. d¨Cf Fractions of cellular lysates were utilized to analyze levels of Bcl-2, Bcl-xL, cleaved Caspase-3 (d); ¦Ã-H2AX (e) and HO-1 (f) by Western blot. ¦Â-Actin was used as an internal control (d¨Cf). In a and c¨Cf: Results are representative of three different experiments. In b: The columns are the mean£¿¡À£¿S.D. of triplicate readings from two different samples. *p£¿<£¿0.05 compared with vehicle-treated control cells, and #p£¿<£¿0.05 compared with cells treated with sorafenib alone. In d, the bar graphs under the Western blots represent the relative expression Bcl-2/Bcl-xL/Caspase-3 (cleaved) by densitometry, where the signals were normalized to the expression of an internal control ¦Â-Actin. The columns represent the average£¿¡À£¿S.D of relative intensities from three different blots. *p£¿<£¿0.05 compared with cells treated with sorafenib alon %K Apoptosis %K Cancer therapeutic resistance %U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333845/