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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.

Reprimo as a modulator of cell migration and invasion in the MDA-MB-231 breast cancer cell line