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. 2019 Jul 9;18(3):2694–2703. doi: 10.3892/ol.2019.10589

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Copyright: © Li et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — p70S6K knock down enhances the anti-proliferative effects of Doxo in K562 cells. K562 cells were cultured and transfected with p70S6K targeting siRNA for 48 h. Successful knockdown of p70S6K was confirmed by (A) RT-qPCR and (B) western blot assays. The results showed that targeting siRNA significantly decreased the expression of p70S6K, compared with the control siRNA group. *P<0.05. Data were presented as mean ± SD of triplicates. (C) Cells were cultured with Doxo (0.5 µM) after p70S6K knockdown, the cell viability was determined by Cell Counting Kit-8. The exposure of p70S6K knockdown and doxorubicin alone or combination significantly inhibited cell viability. *P<0.05. The values are represented as the mean ± SD. The expression of cell cycle molecules were detected using (D) western blotting and (E) RT-qPCR. The expression of CDK4, CDK6, cyclin B1 and cyclin D1 were significantly decreased in p70S6K knockdown and Doxo treatment group compared withthe single treatment group and the control group. *P<0.05. Data were presented as mean ± SD of triplicates. CDK, cyclin dependent kinases; SD, standard deviation; RT-q, reverse transcription-quantitative; si, small interfering; Doxo, doxorubicin; p70S6K, ribosomal protein S6 kinase.