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胰腺癌是一种预后极差的恶性消化道肿瘤，5年生存率小于5%，这与胰腺癌细胞的凋亡异常有着密切的关系。Bad 基因是 Bcl-2 家族中的一种促凋亡基因，被认为可以通过浓度依赖性方式替换Bcl-xL/Bax、Bcl-2/Bax 二聚体中的Bax，从而达到促进细胞凋亡、防止胰腺癌的发生。Bad 基因在胰腺癌中的调控主要以磷酸化/去磷酸化调控最为常见，研究显示，胰腺癌中Bad 表达总量变化不明显，而在Ser112 位点上的磷酸化为灭活的pBad112 形式表达却明显增多。胰腺癌中过表达的14-3-3sigma、Pim-3、 cAMP等均可诱导Bad 蛋白磷酸化，而PKC、MAP4K3等可诱导其去磷酸化。同时，针对Bad 的靶向治疗在胰腺癌中的应用研究已经有所进展，其中有研究发现人参皂苷Rg3、Cantharidin、Stemonamid 等药物均可通过Bad 途径促胰腺癌细胞凋亡。对胰腺癌中的Bad 的深入研究，有利于了解其与胰腺癌发病机制的关系，为胰腺癌的靶向治疗提供新的方向。

英文摘要:

Pancreatic cancer is a malignant gastrointestinal tumors of poor prognosis, and the 5-year survival rate of pancreatic cancer is less than 5%.It has a close relationship with the apoptosis of pancreatic cancer cells. Bad gene is one of the members of the Bcl-2 family pro-apoptotic genes, which is considered to replace Bax of Bcl-xL/Bax, Bcl-2/Bax dimers of Bax by concentration dependent manner. The most common control of Bad gene in pancreatic cancer is mainly by phosphorylation / dephosphorylation. The research shows that the total Bad expression of pancreatic cancer doesn't change significantly, but the expression of pBad112, which is considered as the form Bad phosphorylated at Ser112 site, is significantly increased. The overexpression of 14-3-3sigma, Pim-3, cAMP, etc, can induce Bad phosphorylation. In addition, PKC,MAP4K3, etc, can induce the dephosphorylation of the Bad. Meanwhile, several researches progress have been made in the field the research of the targeted therapy to Bad in pancreatic cancer, which shows that ginsenoside Rg3, Cantharidin, Stemonamid and others are available to promote pancreatic cancer cell apoptosis through Bad pathway. The penetrating research of Bad in pancreatic cancer may help us to acknowledge the relationship between Bad and the pathogenesis of pancreatic cancer cells, which may lead to a new trend in the targeted therapy of pancreatic cancer.

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