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. 2019 Dec 16;43(2):525–535. doi: 10.3892/or.2019.7438

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Copyright: © Cui 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 6. — XIST regulates IRS1 expression and the PI3K/AKT signaling pathway via inhibition of miR-144. (A) IRS1 mRNA expression was determined in TU212 cells transfected with sh-NC, sh-XIST and sh-XIST+anti-miR-144. (B) IRS1, PI3K, p-PI3K, AKT and p-AKT protein levels were assessed in TU212 cells transfected with sh-NC, sh-XIST and sh-XIST+anti-miR-144. (C) IRS1 mRNA expression was examined in LSCC tissues and adjacent normal tissues (n=48) by reverse transcription-quantitative PCR. (D) Correlation between XIST expression and IRS1 expression in LSCC tissues was analyzed by Pearson's correlation analysis. *P<0.05, **P<0.01. LSCC, laryngeal squamous cell carcinoma; IRS1, insulin receptor substrate 1; XIST, X inactive-specific transcript; NC, negative control.