Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2019 Nov 26;39(9):1983–1996. doi: 10.1038/s41388-019-1120-z

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 6 — miR-200a inhibited miR-16 expression, therefore reducing miR-16 binding to 3′-UTR of JNK2 mRNA, and increasing JNK2 protein translation. a JNK2 3′-UTR activity was evaluated by transfection of JNK2 3′-UTR-driven luciferase reporter along with pRL-TK into transfectants as indicated. Bars represent means ± SD from three independent experiments. b miRNA expression levels were evaluated by real-time PCR in T24T(Vector) vs. T24T(miR-200a) cells. Results were normalized to U6. c miRNA expression levels were evaluated by real-time PCR in T24T(Vector) vs. T24T (miR-200a inhibitor) cells. Results were normalized to U6. d Schematic of miR-16 binding site in JNK2 mRNA 3′-UTR region and its mutants aligned with miR-16. e T24T(Vector) and T24T(miR-200a) cells were co-transfected with wild-type and mutant JNK2 3′-UTR luciferase reporters and pRL-TK, respectively. Luciferase activity of each transfectant was evaluated and results were presented as relative JNK2 3′-UTR activity. f Real-time PCR was used to identify the miR-16 expression in T24T(miR-200a/Vector) vs. T24T (miR-200a/ miR-16) cells. Bars represents means ± SD from three independent experiments. g Extracts from T24T (miR-200a/ Vector) vs. T24T (miR-200a/ miR-16) cells were used to evaluate effect of miR-16 on expression of JNK1, JNK2, p-c-Jun, c-Jun, and MMP-2 by western blot. β-Actin was used as protein loading control. Results shown are representative of three independent experiments. Invasion abilities of T24T(miR-200a/Vector) and T24T(miR-200a/miR-16) cell were evaluated using Invasion Chambers (h); and the relative invasion ability was plotted (i). Bars represent means ± SD from three independent experiments. j Real-time PCR was used to identify the miR-16 expression in T24T(Vector) vs. T24T (miR-16 inhibitor) cells. Bars represents means ± SD from three independent experiments. k Extracts from T24T(Vector) vs. T24T (miR-16 inhibitor) cells were used to evaluate effect of miR-16 on expression of JNK1, JNK2, p-c-Jun, c-Jun, and MMP-2 by western blot. β-Actin was used as protein loading control. Results shown are representative of three independent experiments. Invasion abilities of T24T(Vector) and T24T (miR-16 inhibitor) cell were evaluated using invasion chambers (l); and the relative invasion ability was plotted (m). Bars represent means ± SD from three independent experiments. *p < 0.01, ^#p < 0.05