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. 2022 Sep 26;114(1):152–163. doi: 10.1111/cas.15582

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© 2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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HMGA2 Regulation of AKT activity via IGFBP1 expression. (A–C) Dox‐responsive shRNA HMGA2 #1 and #2‐expressing and the control (NT) cells incubated under Dox (+) or (−) conditions (A), or JHH‐2 (B) and HepG2 (C) cells treated with HMGA2 and the control (Ctr) pooled siRNA were examined by western blotting after 4 days and by qPCR after 3 days. β‐Actin, the loading control. The values represent the mean ± SD from triplicates and are shown relative to the control (Dox + or Ctr) after normalizing the corresponding values to TATA‐box binding protein. **p < 0.005; *p < 0.05; n.s., not significant. (D) Cells were treated with IGFBP1 (BP1), IGFBP3 (BP3), and control (Ctr) pooled siRNA for 3 days and analyzed by western blotting.