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. 2017 Feb 20;7:42680. doi: 10.1038/srep42680

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Copyright © 2017, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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(A) The relative proliferation of A549 cells after transfection with equal doses of control agomir, miR-203 agomir, control antagomir or miR-203 antagomir. (B) The relative proliferation of A549 cells after transfection with equal doses of control agomir plus control vector, miR-203 agomir plus control vector, control agomir plus LIN28B vector, or miR-203 agomir plus LIN28B vector. (C and D) A549 cells were transfected with equal doses of control agomir, miR-203 agomir, control antagomir or miR-203 antagomir, or with equal doses of control agomir plus control vector, miR-203 agomir plus control vector, control agomir plus LIN28B vector, or miR-203 agomir plus LIN28B vector. The cell apoptosis profiles were analyzed using flow cytometry. The biparametric histogram shows the cells in early (bottom right quadrant) and late apoptotic states (upper right quadrant). Viable cells are double negative (bottom left quadrant). (C) A representative image; (D) The results of a quantitative analysis. (E) A model of the miRNAs-mediated enhancement of let-7 biogenesis by targeting LIN28B to suppress tumor growth in lung cancer. The results are presented as the means ± SE of three independent experiments (^*P < 0.05, ^**P < 0.01, ^***P < 0.001).