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. 2020 Jun 16;10:915. doi: 10.3389/fonc.2020.00915

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Copyright © 2020 Nie, Qian, Shi, Li, Peng, Ding, Zhang, Zhang, Xu, Lv, Wang, Friess, Kong, Zou and Shen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ALDH1A3 activates the PI3K/AKT pathway and up-regulates HK2 by crosstalking with PPARγ. (A) The promoter regions of HK2 genes contained several PPAR response elements (PPRE). (B) Analyses of data on the cBioPortal showed the expression of HK2 was higher in PPARγ-high expression group compared to that in PPARγ-low expression group (p < 0.0001), and the expression of PPARγ and HK2 showed significant positive correlation (p < 0.0001). (C) ALDH1A3 overexpression in PANC-1 cells up-regulated PPARγ expression while ALDH1A3 knockdown in HPAC cells decreased the expression of PPARγ. (D,E) The PPARγ agonist-Rosiglitazone used in PANC-1 cells could increase lactate production and ATP production, while the PPARγ inhibitor-T0070907 used in HPAC cells could decrease lactate production and ATP production. (F) The PPARγ agonist-Rosiglitazone used in PANC-1 cells could up-regulate the expression of HK2 and PKM2 and activate PI3K/AKT/mTOR signaling pathway, while the PPARγ inhibitor-T0070907 used in HPAC cells could down-regulate the expression of HK2 and PKM2 and suppress PI3K/AKT/mTOR signaling pathway.