Published online Mar 7, 2014. doi: 10.3748/wjg.v20.i9.2335
Revised: December 11, 2013
Accepted: January 8, 2014
Published online: March 7, 2014
Processing time: 150 Days and 4.6 Hours
Pancreatic cancer is one of the most aggressive and difficult cancers to treat. Despite numerous research efforts, limited success has been achieved in the therapeutic management of patients with this disease. In the current review, we focus on one component of morphogenesis signaling, Hedgehog (Hh), with the aim of developing novel, effective therapies for the treatment of pancreatic cancer. Hh signaling contributes to the induction of a malignant phenotype in pancreatic cancer and is responsible for maintaining pancreatic cancer stem cells. In addition, we propose a novel concept linking Hh signaling and tumor hypoxic conditions, and discuss the effects of Hh inhibitors in clinical trials. The Hh signaling pathway may represent a potential therapeutic target for patients with refractory pancreatic cancer.
Core tip: Hedgehog (Hh) signaling is involved in the induction of malignant potential in pancreatic cancer, controlling processes of proliferation, invasiveness and tumorigenesis. This phenotypic change is closely associated with the nuclear factor kappa-light-chain-enhancer of activated B cells transcription factor, both in an autocrine and paracrine manner. Hh signaling is also capable of maintaining pancreatic cancer stem cells, and may be activated under conditions of tumor hypoxia. Thus, the Hh signaling pathway may represent a potential therapeutic target for patients with refractory pancreatic cancer and the use of Hh inhibitors will likely play an important role in future therapeutic strategies.