Abstract Aims: We aimed to investigate the role of estrogen-development signal in growth of gastric cancer cell, and the expression and location change of new estrogen receptor ER-α36 in gastric cancer cell when dealt with estrogen. Methods: Gastric cancer BGC823 was chosen as research model and 17β- estradiol (E2) was used to deal with cell. Cell growth was examined by WST-1 method and assayed by microplate reader. ER-α36 expression in mRNA and protein level was assayed by RT-PCR and Western-blot methods and was quantitated. The location of ER-α36 in cell was examined by immunofluorenscence methods. Result: The cell numbers significantly increased in all E2 treatment groups compared with control group and the number of the cell was more at 48h than 24h in E2 treatment groups (p<0.05), but with E2 concentration increased, cell growth rate slowed down. ER-α36 mRNA expressions of all E2 treatment groups were more than that of control group at 24h and 48h, and had a concentration-dependent of E2 (p<0.05). ER-α36 protein expression had a concentration-dependent of E2 and was less at 48h than 24h in E2 treatment groups (p<0.05). E2 treatment groups’ protein expression were more than control group's at 24h (p<0.05), and were less than control group's at 48h (p<0.05). ER-α36 is localized on the membrane and cytoplasm of BGC823 cell, and its location did not change dealt with E2. Conclusion: E2 could promote the growth of BGC823 cell, and estrogen in different concentration may play different role in the growth regulation of gastric cancer. ER-α36 could response to estrogen-dependent signaling of growth and may transmit it through a membrane-based pathway in gastric cancer. There were regulations in transcription and translation of ER-α36 in gastric cancer. ER-α36 was an important estrogen receptor in gastric cancer and may be a potential predicted marker of gastric cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 147. doi:1538-7445.AM2012-147