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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Sousa de Lacerda, Tonielli Cristina [1, 2] ; Costa-Silva, Bruno [1, 3, 4, 5] ; Giudice, Fernanda Salgueiredo [1] ; Salles Dias, Marcos Vinicios [1] ; de Oliveira, Gabriela Pintar [1] ; Teixeira, Bianca Luise [1] ; dos Santos, Tiago Goss [1] ; Martins, Vilma Regina [1]
Total Authors: 8
[1] AC Camargo Canc Ctr, Int Res Ctr, Rua Tagua 440, BR-01508010 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Inst Chem, Dept Biochem, Av Prof Lineu Prestes, 748 Cidade Univ, BR-05508000 Sao Paulo, SP - Brazil
[3] Weill Cornell Med Coll, Meyer Canc Ctr, Drukier Inst Childrens Hlth, Childrens Canc & Blood Fdn Labs, Dept Pediat, New York, NY 10021 - USA
[4] Weill Cornell Med Coll, Drukier Inst Childrens Hlth, Meyer Canc Ctr, Dept Cell & Dev Biol, New York, NY 10021 - USA
[5] Champalimaud Res, Champalimaud Ctr Unknown, Av Brasilia, P-1400038 Lisbon - Portugal
Total Affiliations: 5
Document type: Journal article
Source: CLINICAL & EXPERIMENTAL METASTASIS; v. 33, n. 5, p. 441-451, JUN 2016.
Web of Science Citations: 4

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. (AU)

Grantee:Bianca Luise Teixeira
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 13/26097-0 - Analysis of PrPC/STI1 signaling and possible therapeutic role in Amyotrophic Lateral Sclerosis
Grantee:Gabriela Pintar de Oliveira
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 10/19200-1 - Identification of mechanisms of protein STI1/Hop secretion
Grantee:Marcos Vinicios Salles Dias
Support type: Scholarships in Brazil - Post-Doctorate
FAPESP's process: 11/18718-0 - The role of PrPc-HOP complex in colon tumors
Grantee:Tonielli Cristina Sousa de Lacerda
Support type: Scholarships in Brazil - Doctorate (Direct)
FAPESP's process: 09/14027-2 - Mechanisms associated with the function of prion protein and its ligand STI1/Hop: therapeutic approaches
Grantee:Vilma Regina Martins
Support type: Research Projects - Thematic Grants
FAPESP's process: 12/23285-8 - Characterization of extracellular vesicles secreted by cancer cells and evaluation of their role in the progression, metastasis and prognosis of head and neck squamous cell carcinoma
Grantee:Fernanda Salgueiredo Giudice Garcilazo
Support type: Scholarships in Brazil - Post-Doctorate