NDLI: Prion protein binding to HOP modulates the migration and invasion of colorectal cancer cells

Content Provider	Springer Nature Link
Author	Lacerda, Tonielli Cristina Sousa Costa Silva, Bru Giudice, Fernanda Salgueiredo Dias, Marcos Vinicios Salles Oliveira, Gabriela Pintar Teixeira, Bianca Luise Santos, Tiago Goss Martins, Vilma Regina
Copyright Year	2016
Abstract	Colorectal cancer (CRC) is one of the most frequently diagnosed malignancies. The generation of conventional treatments has improved, but approximately 50 % of patients with CRC who undergo potentially curative surgery ultimately relapse and die, usually as a consequence of metastatic disease. Our previous findings showed that engagement of the cellular prion protein (PrPC) to its ligand HSP70/90 heat shock organizing protein (HOP) induces proliferation of glioblastomas. In addition, PrPC has been described as an important modulator of colorectal tumor growth. Here, we investigated the biological relevance of the PrPC-HOP interaction in CRC cells. We demonstrate that HOP induced the migration and invasion of CRC cell lines in a PrPC-dependent manner and that phosphorylation of the ERK1/2 pathway is a downstream mediator of these effects. Additionally, we show that a HOP peptide with the ability to bind PrPC and abolish the PrPC-HOP interaction inhibited the migration and invasion of CRC cells. Together, these data indicate that the disruption of the PrPC-HOP complex could be a potential therapeutic target for modulating the migratory and invasive cellular properties that lead to metastatic CRC.
Starting Page	441
Ending Page	451
Page Count	11
File Format	PDF
ISSN	02620898
Journal	Clinical & Experimental Metastasis
Volume Number	33
Issue Number	5
e-ISSN	15737276
Language	English
Publisher	Springer Netherlands
Publisher Date	2016-04-25
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Prion protein HOP protein Colorectal cancer Invasion Migration Cancer Research Biomedicine general Oncology Hematology Surgical Oncology
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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