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Caveolin-1 Mediates Inflammatory Breast Cancer Cell Invasion via the Akt1 Pathway and RhoC GTPase*

Posted by on in 2015
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Joglekar M1Elbazanti WOWeitzman MDLehman HLvan Golen KL. 2015. J Cell Biochem.

116: 923–933 doi:10.1002/jcb.25025
  • 1The Center for Translational Cancer Research, Dept. of Biological Sciences, The University of Delaware; The Helen F. Graham Cancer Center.


With a propensity to invade the dermal lymphatic vessels of the skin overlying the breast and readily metastasize, inflammatory breast cancer (IBC) is arguably the deadliest form of breast cancer. We previously reported that caveolin-1 is overexpressed in IBC and that RhoC GTPase is a metastatic switch responsible for the invasive phenotype. RhoC-driven invasion requires phosphorylation by Akt1. Using a reliable IBC cell line we set out to determine if caveolin-1 expression affects RhoC-mediated IBC invasion. Caveolin-1 was down regulated by introduction of siRNA or a caveolin scaffolding domain. The ability of the cells to invade was tested and the status of Akt1 and RhoC GTPase examined. IBC cell invasion is significantly decreased when caveolin-1 is down regulated. Activation of Akt1 is decreased when caveolin-1 is down regulated, leading to decreased phosphorylation of RhoC GTPase. Thus, we report here that caveolin-1 overexpression mediates IBC cell invasion through activation Akt1, which phosphorylates RhoC GTPase. This article is protected by copyright. All rights reserved.

*Note: The anti-IgY agarose used in this publication was manufactured by Gallus Immunotech Inc.



Caveolin-1; Inflammatory breast cancer; Invasion; Metastasis; RhoC GTPase

[PubMed - as supplied by publisher]
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