胰腺癌恶性程度高、预后差，缺乏有效治疗手段，因此通过分子分型实现胰腺癌的个体化治疗具有极其重要的临床意义。基于表达谱水平的分型能较准确地反应各胰腺癌亚组的分子特征，其中Collisson提出的分型得到了较为广泛的认可，而其中的准间质亚组恶性程度最高，亟待进一步研究。我们前期研究发现，AHNAK2作为准间质亚组的标志性基因，在胰腺癌组织中的表达显著升高且与患者的预后密切相关。进一步研究发现，突变型p53蛋白作为转录因子促进了AHNAK2的表达，而高表达的AHNAK2显著增强了胰腺癌的侵袭转移能力及瓦伯格效应。因此我们推测，突变型p53诱导的AHNAK2作为衔接蛋白通过对PKC、PLCγ及mTOR等关键通路分子的调控，促进了胰腺癌的瓦伯格效应。本课题将进一步研究AHNAK2的表达调控及促进有氧糖酵解的分子机制，以期通过我们的研究加深对胰腺癌生物学特征的认识并为其治疗提供新的思路。

Pancreatic cancer is one of the most aggressive cancer, characterized by poor prognosis and treatment resistance. The identification of cancer-specific signature may help us to achieve the precision medicine. Based on the expression profiles, Collisson’s classification characterizes the tumour better than somatic mutations and quasimesenchymal subtype is the most aggressive subtype of pancreatic cancer. We find that AHNAK2, the marker of quasimesenchymal subtype, is overexpressed in pancreatic cancer and acts as an independent prognosis marker. The overexpression of AHNAK2, which is directly induced by mutant p53 protein, promotes the Warburg effect and enhances the ability of migration and invasion. We assume that AHNAK2 enhances the Warburg effect by acting as an adaptor protein to modulate mTOR signaling through the spatial coordination of the PKC/PLCγ and other kinases. We tend to investigate the accurate molecular mechanism of AHNAK2 overexpression thus promoting aerobic glycolysis, which may provide an advanced understanding of the biology behavior of quasimesenchymal subtype and shed insight into potential therapeutic targets for pancreatic cancer.