Show simple item record

dc.contributor.authorLawlor, Garrett
dc.contributor.authorDoran, Peter P
dc.contributor.authorMacMathuna, Padraic
dc.contributor.authorMurray, David W
dc.date.accessioned2011-01-18T11:37:43Z
dc.date.available2011-01-18T11:37:43Z
dc.date.issued2010-06-22
dc.identifierhttp://dx.doi.org/10.1186/1756-9966-29-81
dc.identifier.citationJournal of Experimental & Clinical Cancer Research. 2010 Jun 22;29(1):81
dc.identifier.urihttp://hdl.handle.net/10147/119687
dc.description.abstractAbstract 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.
dc.titleMyeov (myeloma overexpressed gene) drives colon cancer cell migration and is regulated by PGE2
dc.typeJournal Article
dc.language.rfc3066en
dc.rights.holderLawlor et al.; licensee BioMed Central Ltd.
dc.description.statusPeer Reviewed
dc.date.updated2010-12-16T13:01:06Z
refterms.dateFOA2018-08-22T10:29:52Z
html.description.abstractAbstract 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 &#956; M, 0.1 &#956; M and 1 &#956; 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 &lt; 0.05) with a 39% reduction compared to control at 36 hours (p &lt; 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% &amp; 1,000% increase in Myeov expression for 0.00025 &#956; M, 0.1 &#956; M and 1 &#956; 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.


Files in this item

Thumbnail
Name:
1756-9966-29-81.xml
Size:
29.51Kb
Format:
XML
Thumbnail
Name:
1756-9966-29-81.pdf
Size:
429.0Kb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record