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Reprimo as a modulator of cell migration and invasion in the MDA-MB-231 breast cancer cell line.
Buchegger, Kurt; Ili, Carmen; Riquelme, Ismael; Letelier, Pablo; Corvalán, Alejandro H; Brebi, Priscilla; Huang, Tim Hui-Ming; Roa, Juan Carlos.
Afiliação
  • Buchegger K; Department of Pathology, Molecular Pathology Laboratory BIOREN-CEGIN, School of Medicine, Universidad de La Frontera, Temuco, Chile. k.buchegger@gmail.com.
  • Ili C; Department of Pathology, Molecular Pathology Laboratory BIOREN-CEGIN, School of Medicine, Universidad de La Frontera, Temuco, Chile. carmengloriaili@gmail.com.
  • Riquelme I; Department of Pathology, Molecular Pathology Laboratory BIOREN-CEGIN, School of Medicine, Universidad de La Frontera, Temuco, Chile. 83ismode@gmail.com.
  • Letelier P; School of Health Sciences, Universidad Católica de Temuco, Temuco, Chile. pablolete@gmail.com.
  • Corvalán AH; Centre for Translational Research in Oncology (CITO) and Department of Hematology and Oncology, Pontificia Universidad Catolica de Chile, Santiago, Chile. corvalan01@gmail.com.
  • Brebi P; Department of Pathology, Molecular Pathology Laboratory BIOREN-CEGIN, School of Medicine, Universidad de La Frontera, Temuco, Chile. brebimieville@gmail.com.
  • Huang TH; Department of Molecular Medicine/Institute of Biotechnology, University of Texas Health Science Center at San Antonio, STRF, Room 225, 7703 Floyd Curl Drive, San Antonio, TX, 78229, USA. huangt3@uthscsa.edu.
  • Roa JC; Department of Pathology, Advanced Center for Chronic Diseases (ACCDiS) (CITO), School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile. jcroas@gmail.com.
Biol Res ; 49: 5, 2016 Jan 22.
Article em En | MEDLINE | ID: mdl-26796959
BACKGROUND: Reprimo (RPRM), a highly glycosylated protein, is a new downstream effector of p53-induced cell cycle arrest at the G2/M checkpoint, and a putative tumor suppressor gene frequently silenced via methylation of its promoter region in several malignances. The aim of this study was to characterize the epigenetic inactivation and its biological function in BC cell lines. METHODS: The correlation between RPRM methylation and loss of mRNA expression was assessed in six breast cancer cell lines by methylation specific PCR (MSP), 5'-Aza-2'-deoxycytidine treatment and RT-PCR assays. MDA-MB-231 cells were chosen to investigate the phenotypic effect of RPRM in cell proliferation, cell cycle, cell death, cell migration and invasion. RESULTS: In the cancer methylome system (CMS) (web-based system for visualizing and analyzing genome-wide methylation data of human cancers), the CpG island region of RPRM (1.1 kb) was hypermethylated in breast cancer compared to normal breast tissue; more interesting still was that ERα(+) tumors showed higher methylation intensity than ERα(-). Downregulation of RPRM mRNA by methylation was confirmed in MDA-MB-231 and BT-20 cell lines. In addition, overexpression of RPRM in MDA-MB-231 cells resulted in decreased rates of cell migration, wound healing and invasion in vitro. However, RPRM overexpression did not alter cell viability, phosphatidylserine (PS) translocation or G2/M cell cycle transition. CONCLUSION: Taken together, these data suggest that RPRM is involved in decreased cell migration and invasion in vitro, acting as a potential tumor suppressor gene in the MDA-MB-231 cell line.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias da Mama / Glicoproteínas / Movimento Celular / Proteínas de Ciclo Celular / Proliferação de Células Limite: Female / Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias da Mama / Glicoproteínas / Movimento Celular / Proteínas de Ciclo Celular / Proliferação de Células Limite: Female / Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article