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. 2020 Aug 19;11(8):660. doi: 10.1038/s41419-020-02877-0

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© The Author(s) 2020

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/.

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Fig. 7 — a Relative miR-141 expression after transient transfection of miR-141 inhibitor compared to miRNA inhibitor control (miR-CON) in non-malignant RPTEC cells. b Relative expression of CDKN2B-AS1 in miR-141 inhibited RPTEC cells. c miR-141 inhibition in RPTEC cells induced cell proliferation. d Increased colony formation in miR-141 inhibited RPTEC cells as compared to control. e An increase in migration and invasion of miR-141 inhibited RPTEC cells. f, g A significant increase in the mRNA expression of cyclin-D1, cyclin-D2, rac1, paxillin, vimentin, fibronectin (FN1) along with decrease in the expression of α-E-catenin and claudin in RPTEC cells with inhibition of miR-141 compared to control. h Schematic representation showing knockdown of CDKN2B-AS1 due to overexpression of miR-141 results in decreased cyclin-D1 and cyclin-D2 expression which in turn inhibits proliferation/survival/invasion and migration pathways.