Cárdenas P.1,2, López L.1,2, Marchant M.1,2, Corvalán A.2, Guzmán L.1.
1Instituto de Química, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Valparaíso, Valparaíso, Chile; 2Laboratorio de Oncología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.
Introduction: Recent studies show that estrogen (E2) plays a key role in the pathogenesis of gastric cancer (GC). These studies show that E2 enhances tumor proliferation via estrogen receptor (ER) in CG. Malik et al. showed that E2 measured RPRM repression by formation of a RPRM-ERα complex in breast cancer. Based on these results, our group assessed the effect of estrogen on cell proliferation in an AGS RPRM negative (AGS-) cell line and AGS cell line stably transfected with the coding region of RPRM (AGS+). We observed in several experimental tests, using different concentrations of E2, a decrease in cellular proliferation, compared with the control condition [AGS- with E2]. We found a high level of ERβ in clinical samples by immunohistochemistry, indicating a key role in GC. Objectives: Molecular characterization of ERβ in clinical specimens and cell lines. Methods: ERα, ERβ, FOXA1 and RPRM expression was evaluated in GC cell lines (AGS-, AGS+ and KATO III) by RT-PCR. FOXA1 and RPRM levels were detected by Western blot. We evaluated the effect of E2 on proliferation in GC cell lines by CellTiter-Glo®. We detected ERβ by immunohistochemistry on clinical specimen of GC patients. Results: We determined that all lines studied expressed ERα, ERβ, FOXA1 and RPRM. We found that proliferation decreases 53.46% in AGS+ in presence of E2. We found high levels of ERβ on clinical specimens of GC patients. Conclusion: Results suggest that ERβ could be involved in GC development, showing a similar pathway to that of breast cancer, where FOXA1 and RPRM play an important role.