Journal of Cancer Prevention

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pISSN 2288-3649
Fig. 1.

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Fig. 1. Ubiquitin-specific peptidase (USP8) inhibitor suppresses anchorage-independent growth of H1299 and H1650 cells by down-regulation of oncogenic receptor tyrosine kinases. (A) Chemical structure of USP8 inhibitor. (B) Effect of USP8 inhibitor on non-small cell lung cancers (NSCLCs) signaling. H1299 and H1650 cells were treated with the indicated concentrations of USP8 inhibitor for 24 hours to analyze molecular responsiveness. (C) Interaction of epidermal growth factor receptor (EGFR) and USP8 in NSCLCs. Cell lysates from H1299 and H1650 cells were subjected to immunoprecipitation (IP) and western blotting (WB) using the control immunoglobulin G (IgG), EGFR, and USP8 antibodies. (D, E) Colony formation of H1299 and H1650 cells after exposure to the increasing concentration of USP8 inhibitor or gefitinib for 7 days. Random areas were scanned (five areas per well, three wells per set) in colonies grown in soft agar. Error bars represent the mean ± SD. Statistical significance was determined by the Student’s t-test (*P < 0.01).
Journal of Cancer Prevention 2015;20:57~63
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