侵袭转移是导致胃癌患者死亡的首要因素，其中上皮-间质转化（EMT）是上皮来源肿瘤侵袭转移的重要机制。表观遗传学调控是EMT和侵袭转移研究领域的重要科学问题。本课题组研究发现表观遗传分子组蛋白去甲基化酶JMJD2B在胃癌细胞中影响EMT关键分子的表达，干扰JMJD2B的表达显著抑制胃癌细胞的迁移能力并诱导细胞形态的转变,提示JMJD2B在EMT和胃癌侵袭转移中的潜在作用。在此基础上，课题组将进一步研究：（1）细胞和分子水平上JMJD2B对胃癌侵袭转移和胃癌干细胞活性的作用及其对EMT的调控机制；（2）体内水平上裸鼠转移模型中JMJD2B对EMT和胃癌侵袭转移的作用；（3）人体组织标本上JMJD2B和EMT关键分子表达的相关性及其与胃癌侵袭转移的相关性。从而阐明JMJD2B作为表观遗传分子在EMT和胃癌侵袭转移中的作用机制，为干预EMT控制胃癌侵袭转移提供理论依据。

Invasion and metastasis is the primary factor leading to the death of patients with gastric cancer. Epithelial-mesenchymal transition (EMT) is the key mechanism to initiate invasion and metastasis of tumors of epithelial origin. The epigenetic regulation is an important scientific issue in the EMT and metastasis research field. Our preliminary study showed that the expression of EMT related markers were regulated by JMJD2B in gastric cancer cells. Moreover, JMJD2B depletion significantly inhibited the migration capacity of gastric cancer cells and induced the morphologic change. The above observation indicated the potential role of JMJD2B in the regualtion of EMT and metastasis of gastric cancer. Based on the previous findings, we will make further investigation on the following aspects: (1) analyze the role of JMJD2B in the invasion and metastasis of gastric cancer and gastric cancer cell stemness as well as the mechanism of JMJD2B on regulating EMT on cellular and molecular level; (2) investigate the biological role of JMJD2B in the invasion and metastasis of gastric cancer in nude mice model; (3) determine the correlation between the expression of JMJD2B and EMT associated molecules as well as the invasion and metastatic status of gastric cancer patients on human tissues. Through the investigation, we aim to clarify the mechanism of JMJD2B on regulating EMT and invasion and metastasis of gastric cancer and provide theoretical basis for the intervention of EMT and the progression of gastric cancer.