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. 2019 Dec 26;19:351. doi: 10.1186/s12935-019-1070-0

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© The Author(s) 2019

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — LINC00511 accelerated the course of GC via declining miR-625-5p expression a, b CCK8 and colony formation assay were performed to estimate the cell proliferation in cells transfected with miR-625-5p mimics. c, d Flow cytometry analysis and TUNEL assays were conducted to measure apoptosis in cells transfected with miR-625-5p mimics. e Western blot assays were used to measure the relevant protein of apoptosis. f, g The effect of miR-625-5p inhibitor and sh-LINC00511#1 were examined by CCK8 and colony formation assay on cell proliferation. h, i The influence of miR-625-5p inhibitor and sh-LINC00511#1 were appraised on the rate of apoptosis in flow cytometry analysis and TUNEL assay. j Relevant proteins of apoptosis were tested in western blot in cells transfected with miR-625-5p inhibitor and sh-LINC00511#1. *P < 0.05, **P < 0.01