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Abstract
BackgroundReprimo (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.MethodsThe 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.ResultsIn 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.ConclusionTaken 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.
Highlights
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
Reprimo is differentially methylated between Breast cancer (BC) and normal control sample tissues The cancer methylome system (CMS) website uses a computational analysis to calculate the average intensity of RPRM CpG island methylation (Start–End: 154042600–154043700, length: 1.1 kb, Chromosome 2) between BC (77) and normal control samples (10) (Fig. 1a)
We found that 48 h post-scratch, the wound was completely closed in MDAMB-231-pCMV6 cells, while in MDA-MB-231-RPRM cells the wound remained open (Fig. 3c)
Summary
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. Loss of proliferation regulation and the activation of invasion and metastasis are considered hallmarks in many cancer types, including BC. These processes are tightly regulated within normal cells. A deregulation in proliferation may occur by several mechanisms, including direct expression of growth factor ligands and receptors by cancer cells or by induction of surrounding normal cells, which permits an uncontrolled proliferation of tumor cells. At this point, the role of tumor suppressor genes that limit growth and proliferation in cancer is important [2]
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