Original Article
Copyright ©2010 Baishideng. All rights reserved.
World J Gastroenterol. Jan 14, 2010; 16(2): 156-166
Published online Jan 14, 2010. doi: 10.3748/wjg.v16.i2.156
Treatment of biliary tract cancer with NVP-AEW541: Mechanisms of action and resistance
Samuel Wolf, Jana Lorenz, Joachim Mössner, Marcus Wiedmann
Samuel Wolf, Jana Lorenz, Joachim Mössner, Marcus Wiedmann, Department of Internal Medicine II, University of Leipzig, Liebigstr. 20, 04103 Leipzig, Germany
Marcus Wiedmann, Department of Internal Medicine I, St. Mary’s Hospital, Gallwitzallee 123-143, 12249 Berlin, Germany
Author contributions: Wiedmann M designed the research and wrote the paper; Wolf S and Lorenz J performed the research; Mössner J analyzed the data and corrected the manuscript.
Supported by Grant No. 934000-258 from Novartis Oncology (to Wiedmann M)
Correspondence to: Dr. Marcus Wiedmann, PhD, Department of Internal Medicine I, St. Mary’s Hospital, Gallwitzallee 123-143, 12249 Berlin, Germany. wiedmann@marienkrankenhaus-berlin.de
Telephone: +49-30-76783251 Fax: +49-30-76783425
Received: September 7, 2009
Revised: November 2, 2009
Accepted: November 9, 2009
Published online: January 14, 2010
Abstract

AIM: To investigate in vitro treatment with NVP-AEW541, a small molecule inhibitor of insulin-like growth factor-1 receptor (IGF-1R), in biliary tract cancer (BTC), since this disease is associated with a poor prognosis due to wide resistance to chemotherapeutic agents and radiotherapy.

METHODS: Cell growth inhibition by NVP-AEW541 was studied in vitro in 7 human BTC cell lines by automated cell counting. In addition, the anti-tumoral mechanism of NVP-AEW541 was studied by Western blotting, cell cycle analysis and reverse transcription-polymerase chain reaction (RT-PCR). Anti-tumoral drug effect in combination with gemcitabine, 5-fluorouracil (5-FU) and Polo-like kinase 1 inhibitor BI2536 was also studied.

RESULTS: In vitro treatment with NVP-AEW541 suppressed growth in all human BTC cell lines, however response was lower in gallbladder cancer. Treatment with NVP-AEW541 was associated with dephosphorylation of IGF-1R and AKT. In contrast, phosphorylation of p42/p44 and Stat3 and expression of Bcl-xL were inconsistently downregulated. In addition, treated cells showed cell cycle arrest at the G1/S-checkpoint and an increase in sub-G1 peak. Moreover, IGF-1R and its ligands IGF-1 and IGF-2 were co-expressed in RT-PCR, suggesting an autocrine loop of tumor cell activation. Combined with gemcitabine, NVP-AEW541 exerted synergistic effects, particularly at low concentrations, while effects of combination with 5-FU or BI 2536 were only additive.

CONCLUSION: Our findings suggest that NVP-AEW541 is active against BTC in vitro and potentiates the efficacy of gemcitabine.

Keywords: Tyrosine kinase inhibitor, Cholangiocarcinoma, Gemcitabine, NVP-AEW541