Overexpression of Calreticulin Contributes to the Development and Progression of Pancreatic Cancer

摘要: We studied the clinicopathological significance for Calreticulin (CRT) expression in pancreatic cancer (PC), and its functional relationship with other signaling genes (especially p53) regulating biological behavior of PC cells. IHC, IF, IB, real-time PCR were used to detect CRT PC, while transfection drug intervention investigate genes. IHC showed both p53 was significantly increased compared that paired non-cancerous tissues (P < 0.001). High positively associated tumor UICC stage lymph nodes metastasis (P = 0.034 P = 0.015), an independent adverse prognostic indicator patients PC. No found between spearman's rank correlation test. Altered did not change p53, MDM2, pho-AKT, pho-p38, pho-JNK expression, but had a specific regulation on pho-ERK. Meanwhile, CRT-regulated cell proliferation, migration, invasion cells MEK/ERK pathway dependent manner. In addition, knockdown decreased pho-ERK chemoresistance activated caspase-3-related apoptosis gemcitabine- or oxaliplatin-treated Capan-2 Our study first demonstrated overexpression contributed development progression through MEK/ERK-signaling p53. The interaction might provide new idea revealing malignant biology supplying gene targeted chemotherapy