Diana Alrumhi , Loftus P and Barkley L
NUI Galway, Ireland
Posters & Accepted Abstracts: J Cancer Sci Ther
Introduction: Syndecan-2(Sdc-2) is a transmembrane heparin sulfate proteoglycan that is upregulated in breast tumours. Preliminary data indicate that overexpression of Sdc2 peptides in BCCâ??s increases their migratory and immunosuppressive properties. Sdc-2 fragments were designed and cloned into a vector to mimic a component of endogenous Sdc-2. Overexpression of TGF-β results in pro-tumorigenic modifications to cells in the tumour microenvironment. Therefore, inhibition of the TGF-β pathway would be a rational approach in breast cancer therapies. Our objective was to determine the role of Sdc-2 in the TGF-β pathway in MDA-MB-231 BCCâ??s. Method: Cultured MDA-MB-231 breast cancer cells were transfected with Fc empty vector, Sdc-F1 or Sdc-F2. A serum starvation and a TGF-β3 time course were carried out. RNA was harvested from the cells at 0, 1, 2, 4, 6 after TGF- β3 treatment. The RNA was purified and quantified, followed by cDNA synthesis via reverse transcription. qPCR was carried out to determine the effect of Sdc-2 fragments on TGF-β induced genes such as SMAd7, Serpine1 and CTGF. Results: Promising data was collected from all three experiments, however, due to the sensitivity of qPCR the figures were different preventing statistical significance. Throughout all three experiments, consistent trends were observed such as SMAD7 and Serpine1 downregulation by Sdc-2-Fc-peptides indicating TGF-β suppression, especially at the 6 hour time point. Conclusions: Further investigation of Sdc-2-Fc-peptides is imperative since data collected revealed Sdc-2 interaction with TGF-β induced genes.
E-mail: d.alrumhi1@nuigalway.ie
Cancer Science & Therapy received 3968 citations as per Google Scholar report
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