Literature DB >> 18512153

Sorafenib triggers antiproliferative and pro-apoptotic signals in human esophageal adenocarcinoma cells.

Jorge-Shmuel Delgado1, Reba Mustafi, Jason Yee, Sonia Cerda, Anusara Chumsangsri, Urszula Dougherty, Lev Lichtenstein, Alessandro Fichera, Marc Bissonnette.   

Abstract

BACKGROUND AND
PURPOSE: Current therapies offer scant benefit to patients with advanced esophageal adenocarcinoma. We investigated the effects of Sorafenib, a multifunctional kinase inhibitor, on several growth regulatory pathways that control cell growth and survival in SEG-1 cells derived from Barrett's adenocarcinoma.
METHODS: SEG-1 cells were exposed to acidified medium or taurocholic acid, with and without pre-incubation with Sorafenib. Cyclin D1 and E, c-Myc, and Bcl-2 expression levels as well as STAT3 activations were determined by Western blotting. Cyclin D1 mRNA was measured by real-time PCR. Apoptosis was assessed by TUNEL assay.
RESULTS: Sorafenib significantly inhibited SEG-1 cell proliferation stimulated by acid or bile acid treatments and reduced cell survival. This drug significantly reduced the up-regulations of cyclin D1, cyclin E, c-Myc, and Bcl-2 as well as the activation of STAT3 in SEG-1 cells.
CONCLUSIONS: These results support a rational basis for future clinical studies to assess the therapeutic benefit of Sorafenib in esophageal adenocarcinoma.

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Year:  2008        PMID: 18512153     DOI: 10.1007/s10620-008-0294-y

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


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