如何早期检测白斑癌变，判定癌变预后并寻找治疗靶标是临床亟待解决的难题，发现癌变关键分子是核心。内质网I型跨膜蛋白Calnexin是重要的类凝集素分子伴侣，含人鼠高度保守结构域。预实验显示其与口腔鳞癌不良预后相关，可与巨噬细胞和T淋巴细胞结合，并可抑制T淋巴细胞增殖，显示其可能具肿瘤免疫编辑新功能。由此设想：作为伴侣分子，Calnexin可与Calreticulin协同促进肿瘤"eat me signal"功能，且与CD47肿瘤逃逸相互平衡而影响肿瘤行为。也可独立作用于T淋巴细胞诱导肿瘤逃逸。我们将通过分析Calnexin临床表达与预后，沉默该基因观察口腔鳞癌细胞体内外生物学表型，及行人、鼠Calnexin通过巨噬细胞或T淋巴细胞调控肿瘤免疫杀伤或逃逸的体内外研究，并拟用受体芯片系统筛选鉴定CalnexinT细胞表面受体，从而全面揭示Calnexin为核心的肿瘤免疫编辑调控肿瘤发生转移的机理

How to detect malignant transformation of oral leukoplakia in early stage and predict prognosis and finally find effective targeted drugs are urgently needed to be solved in clinical. Pivotal molecules in the developing of oral cancer is the key to uncover the mechanism of canceration and develop the targeted medicine. Calnexin is type I transmembrane protein in endoplasmic reticulum, a class lectin molecular chaperone, containing highly conservative rat domain structure. Our previous proteomic study showed that the total proteins and its phosphorylation are highly expressed in tumor. preliminary experiments displayed that it can combine with T lymphocytes and inhibit its proliferation, which prompted that calnexin is responsible for influencing biological types of cancer epithelial intracellularlly, and affect the function of T lymphocytes and macrophages through intracellular to cell membrane, although the mechanism is unclear. Therein, we hypothesized that calnexin interact with calreticulin as molecular chaperone to promote the function of "eat me signal", and influencing the tumor behavior through balancing tumor escape of CD47. It can also act on T lymphocytes to induce tumor killing or escaping. We will observe biological behavior of tumor epithelial by analyzing its expression and prognosis and silencing its gene. Furthermore, we will conduct experiments in human and rat in vivo and vitro to regulate tumor killing and escaping through macrophages. We will utilize the receptor array system to screen and identify calnexin T cell surface receptors.And fully disclose the core value of calnexin in tumor immune editing mechanism in oral tumor environment.