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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 enhances PDAC glycolysis by activating the PI3K/AKT/mTOR pathway. (A–C) Compared to the control group cells, the PANC-1 cells treated with ALDH1A3-overexpression showed a significant increment in glucose uptake, lactate production, and ATP production, while the HPAC cells treated with ALDH1A3-knockdown showed a decrease in glucose uptake, lactate production and ATP production. (D) ALDH1A3 led to significant enhancement of PI3K/AKT signaling including its downstream targets mTOR.