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. 2017 Sep 12;7:11313. doi: 10.1038/s41598-017-11904-8

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© The Author(s) 2017

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

The signaling pathway for miR-503 playing its EMT-suppressive role in silica-induced pulmonary fibrosis. Silica treatment resulted in the enhanced expression of lncRNA MALAT1, which competitively binding to miR-503 and depressed its expression. When miR-503 was silenced, PI3K p85 binding to miR-503 was released and thereby activated the downstream molecules, thus causing intensified process of EMT.