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. 2020 Jun 16;11(6):466. doi: 10.1038/s41419-020-2671-1

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© The Author(s) 2020

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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Fig. 7 — KLF5 and HDAC1 cooperatively bind on the promoter of IGF1 and suppress IGF1 transcription. KLF5 downregulation in prostate cancer leads to increased IGF1 expression. Subsequently, the autocrine IGF1 activates STAT3 and promotes the expression of its downstream genes, such as MMPs, enhancing the invasive ability of prostate cancer.