Abstract

Recent studies show that estrogen (E2) plays a key role in the pathogenesis of Gastric cancer (GC), where E2 enhances tumor proliferation through estrogen receptor in CG. Malik et al., (2010) show that E2 induces RPRM repression by recruiting of RPRM through ER alpha, in breast cancer. Based on the discussed above, our group assessed the effect of E2 on cell proliferation in a cell line AGS RPRM negative and AGS transfected stably with the coding region of RPRM (AGS RPRM +). ER alpha, ER beta expression and RPRM expression were evaluated in GC cell lines: AGS [RPRM(-) and RPRM(+)], and KATO-III by RT-PCR. We verified the methylation status of the promoter region through bisulfite sequence, in KATO III cells Finally, we have analyzed is the proliferative status by quantification of the ATP present in viable cells. We determined that all lines studied expressed RE alpha and beta and RPRM. In addition, was found that the rate of proliferation decrease a 54 % in AGS (RPRM+) in presence of 3 uM of E2 compared to the condition control AGS (RPRM+). These results suggest that endogenous expression of RPRM could be related with the inhibition of proliferation induced by E2 in gastric cancer cell lines. We should consider to measurement by qRT-PCR, the level expression of RPRM in AGS-RPRM+ cells treated with E2 and analyzed the RPRM protein by Western blot. Grant Support: 0337.460/2012 (PUCV), and Fondecyt-1111014.