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. 2021 Dec;9(24):1798. doi: 10.21037/atm-21-6556

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2021 Annals of Translational Medicine. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

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PTEN was a downstream target of miR-499a-5p. (A,B) The EMT (e-cadherin, n-cadherin, and vimentin) markers of mRNA and protein subjected to miR-499a-5p overexpression or underepxression in PANC1 and Mia-Paca2 cells did not change. (C) Putative binding sites for miR-499a-5p in the PTEN mRNA overexpression or underexpression groups, with the mutated sites being underlined. (D,E) miR-499a-5p overexpression led to a decrease in PTEN at the mRNA and protein level in PANC1 and Mia-Paca2 cells. N=3. (F) miR-499a-5p level modulation in 293T cells exerted a negative regulatory effect on the luciferase activity exhibited by vectors that contained wt 3'-UTR of PTEN relative to vectors that contained MT 3'-UTR. All experiments were repeated 3 times. Data are presented as mean ± SD. ^#, P>0.05; **, P<0.01; ***, P<0.001. PTEN, phosphatase and tensin homolog deleted on chromosome ten; EMT, Epithelial-Mesenchymal Transition; WT, wild type; MT, mutant type; UTR, untranslated region; SD, standard deviation.