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. 2018 Feb 16;11:809–821. doi: 10.2147/OTT.S151867

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© 2018 Zhang et al. This work is published and licensed by Dove Medical Press Limited

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KLK11 silencing activated the PI3K/AKT/apoptosis signaling pathway.

Notes: (A and B) Relative cell viability and relative caspase-3 activity was determined in HCT-8, HCT-8/L-OHP, CON, and KD2 cells. (C) HCT-8/L-OHP induced high expression of PI3K, pAKT, and Bcl-2 proteins, and reduced expression of Bax protein. Moreover, knockdown of KLK11 led to a reduction of PI3K, pAKT, and Bcl-2 and an increase of Bax in HCT-8/L-OHP KD2 cells. Data are presented as mean ± SD of triplicate experiments. **P<0.01 versus HCT-8/L-OHP cell, and versus CON.

Abbreviations: KLK11, kallikrein11; L-OHP, oxaliplatin; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; CON, control groups.