2024-03-29T06:29:34Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/808972016-02-17T15:41:36Zcom_10261_105com_10261_1col_10261_358
2013-08-22T11:40:06Z
urn:hdl:10261/80897
Stromal interaction molecule 2 (STIM2) is frequently overexpressed in colorectal tumors and confers a tumor cell growth suppressor phenotype
Aytes, Álvaro
Morales, Albert
Villanueva, Alberto
Allelic imbalances at chromosome 4p have been largely documented in many different tumor types. In colorectal cancer, loss of heterozygosity (LOH) at 4p15 has been associated with tumor aggressiveness and poor patient outcome, however no target genes in the region have been identified to date. Since stromal interaction molecule 2 (STIM2) is located at 4p15.2 and has been proposed as a candidate gene for this region in glioblastoma multiforme, we aimed at investigating the role of STIM2 in colorectal cancer. We studied STIM2 transcript expression levels in a collection of xenografted primary colorectal tumors (n=20) and a well-annotated tumor series of colorectal cancer (n=140). We observed an overexpression of STIM2 in 63.5% of the cases that was associated with a less invasive phenotype. In vitro and in vivo functional studies with colon cancer cell lines revealed that overexpression of STIM2 reduced cell proliferation and tumor growth, respectively. Our work presents several lines of evidence indicating that STIM2 overexpression is a frequent trait in colorectal cancer that results in cell growth suppression, certifying that even in the absence of somatic genetic or epigenetic alterations, recurrent regions of LOH should still be considered a hallmark for the presence of relevant genes for tumorigenesis. © 2011 Wiley Periodicals, Inc.
2013-08-22T11:40:06Z
2013-08-22T11:40:06Z
2012
2013-08-22T11:40:07Z
artículo
Molecular Carcinogenesis 51(9): 746-753 (2012)
http://hdl.handle.net/10261/80897
10.1002/mc.20843
eng
closedAccess
Wiley-Blackwell