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. 2014 May 6;14:319. doi: 10.1186/1471-2407-14-319

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Copyright © 2014 Sun et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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.

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Downregulation of endogenous GAS5 promotes gastric cancer cell proliferation. (A) MTT assay was performed to determine the proliferation of si-GAS5 transfected MGC803 cells. (B) Colony-forming growth assay was performed to determine the proliferation of si-GAS5 transfected MGC803 cells. (C, D) The effect of GAS5 on gastric cancer cells apoptosis. SGC7901 and BGC823 cells were transfected with pCDNA3.1-GAS5 vector (or empty vector), respectively. Hoechst staining assay for cell apoptosis; the percentage of Hoechst-positive nuclei per optical field (at least 50 fields) was counted. *P < 0.05.