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. 2016 Aug 29;9:5349–5360. doi: 10.2147/OTT.S107957

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© 2016 Jiang et al. This work is published and licensed by Dove Medical Press Limited

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Effects of WP1066 on the JAK2/STAT3 pathway and CHOP resistance induced by ALDH1A1 overexpression.

Notes: (A) The protein levels of ALDH1A1, JAK2/p-JAK2, STAT3/p-STAT3, and pathway targets (Bcl-2, cyclin D1) were assayed by Western blotting. GAPDH was used as an internal control. (B) The IC50 values of CHOP were determined by CCK8 assay. (C) Colony formation assay was performed to determine the long-term effects of WP1066. (D) Flow cytometric analysis of apoptosis in cells combined with CHOP (0 and 640 ng/mL). Data are expressed as the mean ± SD of three individual experiments. *P<0.05.

Abbreviations: ALDH1A1, aldehyde dehydrogenase 1A1; SD, standard deviation; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; CCK-8, Cell Counting Kit-8; CHOP, combinatorial cyclophosphamide, doxorubicin, vincristine, and prednisone; shRNA, short hairpin RNA; Pfeiffer-NC, cells transfected with empty vector; Pfeiffer-shRNA, ALDH1A1-shRNA vector; Pfeiffer-ALDH1A1, ALDH1A1 expression vector; Pfeiffer-ALDH1A1+WP1066, Pfeiffer-ALDH1A1 cells treated with WP1066; p-STAT3, phosphorylated-STAT3; p-JAK2, phosphorylated-JAK2; IC50, half maximal inhibitory concentration.