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. 2015 Oct 29;8:3175–3184. doi: 10.2147/OTT.S91696

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© 2015 Qin et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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Expression of miR-122 reduces the activation of IGF1R/PI3K/AKT signaling pathway.

Notes: A549 (A and B) or H460 (C and D) cells, which were infected with Ad-control or Ad-122, were harvested and analyzed by Western blot assays. The protein level of IGF1R, PI3K catalytic subunit P110, phospho-P110, AKT, and phospho-AKT was detected by antibodies. Relative expression level was shown as mean ± SD from triplicate experiment with similar results (B and D). A549 (E) or H460 (F) cells, which were infected with Ad-control or Ad-122, were co-transfected with SBE-Luc reporters. Cells were harvested and analyzed for luciferase analysis. The relative luciferase activity was shown as mean ± SD from triplicate experiment with similar results (E and F). *P<0.05 versus Ad-control or Ad-122.

Abbreviations: IGF1R, insulin-like growth factor 1 receptor; GAPDH, glyceraldehyde phosphate dehydrogenase; SD, standard deviation; PI3K, phosphatidylinositol 3 kinase.