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. 2017 Apr 12;18:58. doi: 10.1186/s12931-017-0546-5

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — CD44/HA interaction in tumor. CD44/HA binding in the malignant setting elicits an interaction of CD44 with ErbB2, EGFR and TGFßR1 that alter the physiological effects of these receptors. It transmits signals through the cytoplasmic domain after binding with diverse cytoskeletal proteins such as actin-cytoskeleton adaptor protein, ankyrin, ezrin-redixin-moesin (ERM) proteins, intracellular signaling components including the Rho family GTPases, Src kinases and associated molecules. To a great extent, MAP kinase and PI3 kinase/AKT signaling mediate cell proliferation, cell survival, cell motility and invasion as well chemoresistance [14]. ErbB2, epidermal growth factor receptor-2, EGFR, epidermal growth factor receptor, TGFßR1, transforming growth factor beta receptor 1, GTPases, family of hydrolase enzymes that bind and hydrolyse guanosine triphosphate (GTP)