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. 2019 Jan 10;10(1):30. doi: 10.1038/s41419-018-1265-7

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© The Author(s) 2018

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. 3 — As a signal integration platform, the ectodomain of the CD44v6 molecule can be bound with several cytokines, such as EGF, HGF, VEGF, and CXCL12, which are known to be potent in inducing cell proliferation, anti-apoptosis, migration, and angiogenesis through activating MAPK/ERK signaling pathway (red line) and PI3K/Akt signaling pathway (yellow line) after binding with their receptors. Moreover, due to the existing crosstalk between PI3K/Akt and Wnt/β-catenin (see ref. ⁵⁸), β-catenin translocates into the nucleus to promote the expression of EMT-associated genes, thus enabling the invasive and metastasis capabilities of CRC cells to be improved (green line)