2017年9月BMC Cancer杂志(JCR医学二区期刊)上发表了叶建新、黄金胜题目为“ERp29 controls invasion and metastasis of gastric carcinoma by inhibition of epithelial-mesenchymal transition via PI3K/Akt signaling pathway”的研究论文，揭示了ERp29通过PI3K/Akt信号通路调控EMT抑制胃癌细胞侵袭和转移的能力。

胃癌是全球第四常见的恶性肿瘤，其致死率在所有恶性肿瘤位居前列。研究调节胃癌发生及发展的分子信号机制有助于提高胃癌的诊疗水平，是目前胃癌研究的重点。已有报告表明内质网蛋白29（endoplasmic reticulumprotein 29，ERp29）可以抑制乳腺癌的进展，但是其在胃癌中的作用仍不明确。本文首先发现ERp29在胃癌组织中较癌旁组织表达下调，且其在胃癌组织中低表达与患者的不良临床预后相关。随后一系列的体内外实验证实ERp29可调控胃癌细胞侵袭、转移和EMT，该效应通过ERp29抑制AKT信号通路实现。这些研究表明ERp29可做为胃癌诊断及治疗的新靶点。

叶建新、黄金胜为本文共同第一作者，林旭，李筠为本文通讯作者，徐杰，黄强，王锦洲，钟文进，林心建参与了该课题的研究。该项目得到了福建省卫计委中青年骨干人才项目和福建省自然基金项目的资助。

Fig. 5 Regulation of EMT by ERp29 was dependent on PI3K/Akt pathway. (a) GSEA plot showing that ERp29 expression negatively correlated with Akt-activated gene signatures (REACTOME_PI3K_AKT_ACTIVATION) and positively correlated with GSK3β-pathway (BIOCARTA_GSK3_PATHWAY) (left panel). Western blot analysis of total Akt, pAKT(Ser473), pAKT(Thr308), GSK-3β and pGSK3β(Ser9) expression in the indicated gastric cancer cell lines. (b) GSEA plot showing that ERp29 expression negatively correlated with Akt/mTOR pathway (MTOR_UP.N4.V1_UP,MTOR_UP.N4.V1_DN).Western blot analysis of mTOR, p-mTOR expression in indicated gastric cancer cell lines. (c) LY294002 and rapamycin reversed the effect of ERp29 overexpression on the cell migratory and invasive abilities. (d) CHIR99021 reversed the effect of ERp29 knockdown on the cell migratory and invasive abilities. *P < 0.05.