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. 2020 May 12;44(1):103–114. doi: 10.3892/or.2020.7611

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Copyright: © Yan 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 5. — Inhibition of KRT17 suppresses the AKT/mTOR/HIF1α pathway. (A-C) The expression of AKT, p-AKT, mTOR, p-mTOR and HIF1α in the sh-scramble and sh-KRT17 groups was detected using western blotting. β-actin was used as a loading control. (D) The co-expression relationship between KRT17 and HIF1α in osteosarcoma tissues was determined using RT-qPCR and Pearson's correlation analysis. (E and F) The mRNA levels of VEGF, GLUT1 and MCL1 were determined using RT-qPCR in the sh-scramble and sh-KRT17 groups. (G-I) The protein levels of VEGF, GLUT1 and MCL1 were detected using western blotting in the sh-scramble and sh-KRT17 groups. *P<0.05, **P<0.01. KRT17, keratin 17; sh, short hairpin; p-, phosphorylated; HIF1α, hypoxia-inducible factor 1α; MCL1, MCL1 apoptosis regulator, Bcl2 family member; GLUT1, glucose transporter 1.