CDCP1 in Breast Cancer
Redaktion
Für den Inhalt der Angaben zeichnet die Projektleitung verantwortlich.
Kooperation
Dieses von der GEBERT RÜF STIFTUNG geförderte Projekt wird von folgenden weiteren Projektpartnern mitgetragen: Friedrich Miescher Institute, Basel
Projektdaten
- Projekt-Nr: GRS-026/11
- Förderbeitrag: CHF 54'000
- Bewilligung: 23.06.2011
- Dauer: 11.2011 - 08.2012
- Handlungsfeld: Pilotprojekte, 1998 - 2018
Projektleitung
- Dr. Mohamed Bentires-Alj
- Friedrich Miescher Institute for Biomedical Research
- Signaling and Cancer
- Maulbeerstrasse 65
- 4058 Basel (Schweiz)
- bentires@fmi.ch
Projektbeschreibung
Each year, approximately 1.3 million women are diagnosed with breast cancer worldwide and more than 410,000 lives are lost to this disease. Although some patients do well after surgery and initial treatment, drug resistance often occurs and tumors relapse. An improved understanding of breast cancer initiation and progression, drug resistance and the factors determining metastatic spread is urgently needed. New therapies are likely to result from a more thorough understanding of the differentiation program of the cells originating the cancer; the genetic and epigenetic alterations that transform these cells; the metabolism of cancer cells, and their interactions with the stroma.
Our project focuses on the roles of the CUB domain-containing protein 1 (CDCP1), a cell surface glycoprotein known to interact with Src family kinase (SFK) and protein kinases C (PKC ), in breast cancer. This work will be undertaken at the Friedrich Miescher Institute in Basel.
Our project focuses on the roles of the CUB domain-containing protein 1 (CDCP1), a cell surface glycoprotein known to interact with Src family kinase (SFK) and protein kinases C (PKC ), in breast cancer. This work will be undertaken at the Friedrich Miescher Institute in Basel.
Was ist das Besondere an diesem Projekt?
This project will assess the merits of CDCP1 as a target in breast cancer.
Stand/Resultate
We assessed the expression of CDCP1 by immunohistochemistry and found that CDCP1 is overexpressed in a subset of human primary breast tumors. We then designed an inducible shRNA targeting CDCP1. Immunoblotting showed that activation of the shRNA depleted CDCP1. We then tested the effect of CDCP1 knockdown in breast cancer cell lines grown as xenografts. We found that Knockdown of CDCP1 after overt tumor development did not affect tumor growth suggesting that CDCP1 is not essential for tumor maintenance.
Publikationen
None
Medienecho
None
Links
Am Projekt beteiligte Personen
Nicola Aceto nicola.aceto@fmi.ch
Letzte Aktualisierung dieser Projektdarstellung 17.10.2018