Role of Wnt/β-catenin Signaling in Drug Resistance of Pancreatic Cancer

被引:128
|
作者
Cui, Jiujie [2 ,3 ]
Jiang, Weihua [2 ,3 ]
Wang, Shuyi [2 ,3 ]
Wang, Liwei [2 ,3 ]
Xie, Keping [1 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal, Unit 426, Houston, TX 77030 USA
[2] Shanghai Jiao Tong Univ, Dept Med Oncol, Shanghai Peoples Hosp 1, Sch Med, Shanghai 200080, Peoples R China
[3] Shanghai Jiao Tong Univ, Shanghai Key Lab Pancreat Dis, Shanghai Peoples Hosp 1, Sch Med, Shanghai 200080, Peoples R China
关键词
Wnt/beta-catenin signaling; angiogenesis; chemoresistance; pancreatic cancer; MEDIATES RADIATION-RESISTANCE; CYCLIN D1 EXPRESSION; BETA-CATENIN; CONTACT INHIBITION; WNT PATHWAY; CELLS; GEMCITABINE; GROWTH; CHEMOTHERAPY; APOPTOSIS;
D O I
10.2174/13816128112092464
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Pancreatic cancer is characterized by its intrinsic resistance to cytotoxic agents. But the underlying molecular mechanism is unclear. Studies demonstrate that angiogenesis, presence of highly resistant cancer stem cells (CSCs), dysregulation of cell cycle and apoptosis are main aspects of mechanisms of pancreatic cancer chemoresistance. Interestingly, recent investigations of Wnt/beta-catenin signaling suggest roles for the signaling in these four aspects and the pathogenesis of pancreatic cancer. Conceivably, the dysregulation of Wnt/beta-catenin signaling pathway is involved in pancreatic cancer chemoresistance. Though researchers have proven it in some other cancer types, however, there is no direct evidence for this reasoning in pancreatic cancer. Designing effective experiment setups to define the function and mechanism of Wnt/beta-catenin signaling in pancreatic cancer chemoresistance and subsequently targeting the signaling to improve the sensitivity of chemotherapy in pancreatic cancer require a full understanding of the molecular mechanisms of Wnt/beta-catenin signaling pathway in angiogenesis, maintaining of highly resistant CSCs, regulation of cell cycle and apoptosis in pancreatic cancer.
引用
收藏
页码:2464 / 2471
页数:8
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