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. 2019 Sep 10;9:12973. doi: 10.1038/s41598-019-49480-8

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© The Author(s) 2019

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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Knockdown of PDK1 plus CPT significantly reduces liver metastasis in CRC by downregulating the adherence capacity via inhibiting STAT3-p-Y705. (A) Transwell assay showed that the knockdown of PDK1 or the combination of CPT and silencing PDK1 significantly decreased migration capacity of liver metastatic HCT116 cells. (B) Histogram indicated the corresponding comparison of migration capacity presented in (A). (C) The liver metastatic HCT116 cells were seeded into a 6-well plate coated with fibronectin. The adherence assay showed that the knockdown of PDK1 significantly decreased the chemotaxis of liver metastatic HCT116 cells. In particular, the combination of CPT and knockdown of PDK1 resulted in a lowest cell adherence capacity. (D) Histogram indicated the corresponding comparison of the adherent cells presented in (C). Data expressed as mean ± S.D., * represents P < 0.05, ** represents P < 0.01, *** represents P < 0.001, and **** represents P < 0.0001.