1. ¹Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Medisinsk Teknisk Forskningssenter, Trondheim N-7489, Norway
2. ²Oncology Unit, St Olavs Hospital HF, Trondheim, Norway
3. ³Department of Mathematical Sciences, Norwegian University of Science and Technology, Trondheim, Norway
4. ⁴Department of Computer and Information Science, Norwegian University of Science and Technology, Trondheim, Norway

Correspondence: Dr E Hofsli, Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, Medisinsk Teknisk Forskningssenter, Trondheim N-7489, Norway. E-mail: eva.hofsli@ntnu.no

Received 28 October 2004; Revised 23 February 2005; Accepted 28 February 2005.

Abstract

Targeting growth-regulatory pathways is a promising approach in cancer treatment. A prerequisite to the development of such therapies is characterisation of tumour growth regulation in the particular tumour cell type of interest. In order to gain insight into molecular mechanisms underlying proliferative responses in neuroendocrine (NE) gastrointestinal (GI) tumours, we investigated gene expression in human carcinoid BON cells after exposure to gastrin, hepatocyte growth factor (HGF), pituitary adenylate cyclase-activating polypeptide or epidermal growth factor. We particularly focused on gastrin- and HGF-induced gene expression, and identified 95 gastrin- and 101 HGF-responsive genes. The majority of these genes are known mediators of processes central in tumour biology, and a number of them have been associated with poor prognosis and metastasis in cancer patients. Furthermore, we identified 12 genes that were regulated by all four factors, indicating that they may be universally regulated during NE GI tumour cell proliferation. Our findings provide useful hypotheses for further studies aimed to search for new therapeutic targets as well as tumour markers in NE GI tumours.