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首页> 外文期刊>Journal of Cellular Physiology >Overexpression of calreticulin contributes to the development and progression of pancreatic cancer
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Overexpression of calreticulin contributes to the development and progression of pancreatic cancer

机译：超表达calreticulin有助于胰腺癌的开发和发展

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We studied the clinicopathological significance for Calreticulin (CRT) expression in pancreatic cancer (PC), and its functional relationship with other signaling genes (especially with p53) in regulating the biological behavior of PC cells. IHC, IF, IB, and real-time PCR were used to detect CRT expression in PC, while transfection and drug intervention were used to investigate the functional relationship of CRT with other signaling genes. IHC showed both CRT and p53 expression was significantly increased in PC, compared to that in paired non-cancerous pancreatic tissues (P<0.001). High expression of CRT was positively associated with tumor UICC stage and lymph nodes metastasis (P=0.034 and P=0.015), and was an independent adverse prognostic indicator in patients with PC. No relationship was found between CRT and p53 expression in spearman's rank correlation test. Altered expression of CRT did not change p53, MDM2, pho-AKT, pho-p38, and pho-JNK expression, but had a specific regulation on pho-ERK. Meanwhile, CRT-regulated cell proliferation, migration, and invasion of PC cells in MEK/ERK pathway dependent manner. In addition, CRT knockdown significantly decreased pho-ERK expression and cell chemoresistance independent of activated p53 and caspase-3-related apoptosis in gemcitabine- or oxaliplatin-treated Capan-2 cells. Our study first demonstrated that overexpression of CRT contributed to the development and progression of PC through MEK/ERK-signaling pathway but independent of p53. The interaction between CRT and MEK/ERK pathway might provide a new idea for revealing malignant biology and supplying new gene targeted chemotherapy of PC. J. Cell. Physiol. 229: 887-897, 2014.
机译：我们研究了临床病理的意义在胰腺Calreticulin (CRT)表达式癌症(PC),其功能的关系其他信号(尤其是p53)的基因调节PC细胞的生物学行为。包含IHC,如果,IB和实时PCR被用来在电脑检测CRT表达式,而转染被用来研究和药物干预CRT与其他功能的关系信号的基因。表达在PC显著增加,相比,在非配对胰腺组织(P < 0.001)。CRT与肿瘤UICC呈正相关阶段和淋巴结转移(P = 0.034P = 0.015),是一个独立的不利PC患者预后指标。CRT和p53之间的关系被发现斯皮尔曼等级相关的测试表达式。改变的CRT并未改变p53的表达,MDM2、pho-AKT pho-p38 pho-JNK表达式,但对pho-ERK有具体规定。与此同时,CRT-regulated细胞增殖,移民和MEK / ERK入侵电脑的细胞路径依赖的方式。可拆卸的显著减少pho-ERK表达和细胞化学抗性无关的激活p53和caspase-3-related细胞凋亡吉西他滨或oxaliplatin-treated Capan-2细胞。CRT导致了过度的电脑的发展和恶化但独立于p53 MEK / ERK-signaling途径。CRT和MEK / ERK通路之间的交互可能为揭示恶性肿瘤提供一个新的想法生物学和提供新基因的目标化疗的PC。887-897, 2014.

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