Lawlor et al. Journal of Experimental & Clinical Cancer Research 2010, 29:81 http://www.jeccr.com/content/29/1/81 Open Access RESEARCH © 2010 Lawlor et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Research MYEOV (myeloma overexpressed gene) drives colon cancer cell migration and is regulated by PGE 2 Garrett Lawlor 1 , Peter P Doran 2 , Padraic MacMathuna 1 and David W Murray* 2 Abstract Introduction: We have previously reported that Myeov (MYEloma OVerexpressed gene) expression is enhanced in colorectal cancer (CRC) and that it promotes CRC cell proliferation and invasion. The role of Myeov in CRC migration is unclear. ProstaglandinE2 (PGE 2 ) is a known factor in promoting CRC carcinogenesis. The role of PGE 2 in modulating Myeov expression has also not been defined. Aim: To assess the role of Myeov expression in CRC cell migration and to evaluate the role of PGE 2 in Myeov bioactivity. Methods: siRNA mediated Myeov knockdown was achieved in T84 CRC cells. Knockdown was assessed using quantitative real time PCR. The effect of knockdown on CRC cell migration was assessed using a scratch wound healing assay. Separately, T84 cells were treated with PGE 2 (0.00025 μ M, 0.1 μ M and 1 μ M) from 30 min to 3 hours and the effect on Myeov gene expression was assessed using real time PCR. Results: Myeov knockdown resulted in a significant reduction in CRC cell migration, observable as early as 12 hours (P < 0.05) with a 39% reduction compared to control at 36 hours (p < 0.01). Myeov expression was enhanced after treatment with PGE 2 , with the greatest effect seen at 60 mins for all 3 PGE 2 doses. This response was dose dependent with a 290%, 550% & 1,000% increase in Myeov expression for 0.00025 μ M, 0.1 μ M and 1 μ M PGE 2 respectively. Conclusion: In addition to promoting CRC proliferation and invasion, our findings indicate that Myeov stimulates CRC cell migration, and its expression may be PGE 2 dependant. Introduction Colorectal cancer is a heterogeneous disease arising from a complex series of molecular changes [1]. In 1990, Fearon and Vogelstein described the molecular basis of colorectal cancer as a multi-step model of carcinogenesis [2]. The model describes the accumulation of genetic events, each conferring a selective growth advantage to an affected colon cell, including inactivation of tumour suppressor genes and activation of oncogenes. Using a bioinformatics approach we have identified genes with enhanced expression in colorectal cancer tis- sue [3,4]. Myeov, (MYEloma OVerexpressed gene) was initially noted for its association with a subset of multiple myeloma cell lines [4,5] and it has also been implicated in oesophageal squamous cell carcinomas [6] and breast cancer [7]. Myeov is co-amplified with cyclin D1, a known oncogene [5]. We have previously shown Myeov to play a role in gastric cancer cell proliferation and inva- sion [3]. Our group has demonstrated a role for Myeov in the pathogenesis of colorectal cancer (CRC), noting a 20-fold increase in Myeov expression in CRC in comparison with normal colorectal tissue [3]. We have also confirmed that Myeov is upregulated in CRC ex vivo using tissue from normal colonic mucosa, adenomas, and carcinomas [3]. Our In vitro RNA interference/knockdown studies, in which Myeov expression was inhibited, revealed a role for Myeov in driving CRC cell proliferation and invasion. However, the role of Myeov expression in CRC cell migration has not been elucidated. We hypothesise, because of its established role in tumour cell invasion, that Myeov is also important for tumour cell migration. The mechanism underlying Myeov expression remains unclear. * Correspondence: dmurray@mater.ie 2 UCD Clinical Research Centre, UCD School of Medicine & Medical Sciences, UCD, 21 Nelson St, Dublin 7, Ireland Full list of author information is available at the end of the article