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. 2016 Oct 3;36(7):885–898. doi: 10.1038/onc.2016.257

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Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

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PFDN1 knockdown inhibits TGF-β1-mediated EMT and cell motility in lung cancer cells. (a) Stable PFDN1-knockdown A549 cells were generated by lentivirus infection. PFDN1 was examined by immunoblotting. (b and c) PFDN1 knockdown inhibited TGF-β1-induced EMT. PFDN1-knockdown A549 cells were treated with TGF-β1 (2 ng/ml) for 48 h. Cell morphology (b) and levels of N-cadherin and E-cadherin (c) were examined. (d) Cell migration was assessed by a transwell assay. A representative morphology image is shown (upper) and the number of migrated cells per field was determined (lower). (e and f) PFDN1 knockdown inhibited TGF-β1-induced cell migration. Cells were treated with TGF-β1 (2 ng/ml) for the time indicated, the migration of A549 cells was detected by a wound-healing assay (e), and the statistical analysis was assessed to show the migration rate (f). (g) PFDN1 knockdown inhibited anchorage-independent growth in A549 cells, as detected by colony formation in a soft agar assay. A representative image of cell morphology is shown (upper) and number of colonies per 35-mm dish was determined (lower).