title: Stromal interaction molecule 2 (STIM2) is frequently overexpressed in colorectal tumors and confers a tumor cell growth suppressor phenotype.
abstract: 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.
authors: Translational Research Laboratory, Institut Català d'Oncologia-Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain.
authors: Alvaro
authors: A
authors: Aytes
authors: David G
authors: DG
authors: Molleví
authors: Maria
authors: M
authors: Martinez-Iniesta
authors: Marga
authors: M
authors: Nadal
authors: August
authors: A
authors: Vidal
authors: Albert
authors: A
authors: Morales
authors: Ramón
authors: R
authors: Salazar
authors: Gabriel
authors: G
authors: Capellà
authors: Alberto
authors: A
authors: Villanueva
mesh_terms: D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D015815:Cell Adhesion Molecules / Q000235:genetics / Q000378:metabolism*; D049109:Cell Proliferation; D002478:Cells, Cultured; D003106:Colon / Q000378:metabolism / Q000473:pathology; D015179:Colorectal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D004273:DNA, Neoplasm / Q000235:genetics; D016147:Genes, Tumor Suppressor; D006801:Humans; D007124:Immunoenzyme Techniques; D017404:In Situ Hybridization, Fluorescence; D019656:Loss of Heterozygosity; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008819:Mice, Nude; D010641:Phenotype; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071738:Stromal Interaction Molecule 2; D023041:Xenograft Model Antitumor Assays
chemical_list: D015815:Cell Adhesion Molecules; D004273:DNA, Neoplasm; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; C513279:STIM2 protein, human; C525024:Stim2 protein, mouse; D000071738:Stromal Interaction Molecule 2