Cells 2014, 3(1), 129-149; doi:10.3390/cells3010129

Flotillins in Receptor Tyrosine Kinase Signaling and Cancer

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Received: 11 December 2013; in revised form: 11 February 2014 / Accepted: 12 February 2014 / Published: 19 February 2014
(This article belongs to the Special Issue Receptor Tyrosine Kinases)
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract: Flotillins are highly conserved proteins that localize into specific cholesterol rich microdomains in cellular membranes. They have been shown to be associated with, for example, various signaling pathways, cell adhesion, membrane trafficking and axonal growth. Recent findings have revealed that flotillins are frequently overexpressed in various types of human cancers. We here review the suggested functions of flotillins during receptor tyrosine kinase signaling and in cancer. Although flotillins have been implicated as putative cancer therapy targets, we here show that great caution is required since flotillin ablation may result in effects that increase instead of decrease the activity of specific signaling pathways. On the other hand, as flotillin overexpression appears to be related with metastasis formation in certain cancers, we also discuss the implications of these findings for future therapy aspects.
Keywords: cancer; receptor tyrosine kinases; flotillins; metastasis; mitogen activated proteins kinase; insulin; diabetes
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MDPI and ACS Style

Banning, A.; Kurrle, N.; Meister, M.; Tikkanen, R. Flotillins in Receptor Tyrosine Kinase Signaling and Cancer. Cells 2014, 3, 129-149.

AMA Style

Banning A, Kurrle N, Meister M, Tikkanen R. Flotillins in Receptor Tyrosine Kinase Signaling and Cancer. Cells. 2014; 3(1):129-149.

Chicago/Turabian Style

Banning, Antje; Kurrle, Nina; Meister, Melanie; Tikkanen, Ritva. 2014. "Flotillins in Receptor Tyrosine Kinase Signaling and Cancer." Cells 3, no. 1: 129-149.

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