title: ALCAM is indirectly modulated by miR-125b in MCF7 cells.
abstract: MicroRNA (miRNA) deregulation is associated with various cancers. Among an expanding list of cancer-related miRNAs, deregulation of miR-125b has been well documented in many cancers including breast. Based on current knowledge, miR-125b is considered to be a tumor suppressor in breast cancers. While important messenger RNA (mRNA) targets have been defined for miR-125b, here, we aimed to further investigate direct/indirect consequences of miR-125b expression in breast cancer cells by using a transcriptome approach. Upon miR-125b expression, a total of 138 cancer-related genes were found to be differentially expressed in breast cancer cells. While only a few of these were predicted to be direct mRNA targets, majority of the gene expression changes were potentially downstream and indirect effects of miR-125b expression. Among these, activated leukocyte antigen molecule (ALCAM) mRNA and protein levels were found to be highly significantly increased upon miR-125b expression. Given the tumor suppressor role of miR-125b in our model system, upon silencing of ALCAM expression, cell proliferation rate re-increased in miR-125b-expressing cells. While ALCAM's possible context-dependent roles are not clear in breast cancer, a diverse expression pattern of ALCAM mRNA was detected in a panel of breast cancer patient samples. Differentially expressed/regulated cancer-related genes upon miR-125b expression along with the significant increase of ALCAM are of future interest to understand how deregulated expression of miR-125b may have a tumor suppressor role in breast and other cancers.
authors.affiliation: Department of Biology, M.E.T.U., Dumlupınar Bulvarı No: 1, Cankaya, 06800, Ankara, Turkey.
authors.forename: H Begum
authors.initials: HB
authors.lastname: Akman
authors.forename: S Duygu
authors.initials: SD
authors.lastname: Selcuklu
authors.forename: Mark T A
authors.initials: MT
authors.lastname: Donoghue
authors.forename: Shiva
authors.initials: S
authors.lastname: Akhavantabasi
authors.forename: Aysegul
authors.initials: A
authors.lastname: Sapmaz
authors.forename: Charles
authors.initials: C
authors.lastname: Spillane
authors.forename: M Cengiz
authors.initials: MC
authors.lastname: Yakicier
authors.forename: A Elif
authors.initials: AE
authors.lastname: Erson-Bensan
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis* / Q000235:genetics; D001943:Breast Neoplasms / Q000235:genetics* / Q000473:pathology; D015816:Cell Adhesion Molecules, Neuronal / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D005326:Fetal Proteins / Q000096:biosynthesis* / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D006801:Humans; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D020410:Activated-Leukocyte Cell Adhesion Molecule
chemical_list: D015703:Antigens, CD; D015816:Cell Adhesion Molecules, Neuronal; D005326:Fetal Proteins; D035683:MicroRNAs; D012333:RNA, Messenger; C105613:ALCAM protein, human; D020410:Activated-Leukocyte Cell Adhesion Molecule; C531888:MIRN125 microRNA, human