Wnt/β-Catenin Signaling: The Culprit in Pancreatic Carcinogenesis and Therapeutic Resistance.
Monish Ram MakenaHimavanth GatlaDattesh VerlekarSahithi SukhavasiManoj K PandeyKartick C PramanikPublished in: International journal of molecular sciences (2019)
Pancreatic ductal adenocarcinoma (PDAC) is responsible for 7.3% of all cancer deaths. Even though there is a steady increase in patient survival for most cancers over the decades, the patient survival rate for pancreatic cancer remains low with current therapeutic strategies. The Wnt/β-catenin pathway controls the maintenance of somatic stem cells in many tissues and organs and is implicated in pancreatic carcinogenesis by regulating cell cycle progression, apoptosis, epithelial-mesenchymal transition (EMT), angiogenesis, stemness, tumor immune microenvironment, etc. Further, dysregulated Wnt has been shown to cause drug resistance in pancreatic cancer. Although different Wnt antagonists are effective in pancreatic patients, limitations remain that must be overcome to increase the survival benefits associated with this emerging therapy. In this review, we have summarized the role of Wnt signaling in pancreatic cancer and suggested future directions to enhance the survival of pancreatic cancer patients.
Keyphrases
- stem cells
- epithelial mesenchymal transition
- cell proliferation
- cell cycle
- free survival
- end stage renal disease
- case report
- ejection fraction
- chronic kidney disease
- newly diagnosed
- gene expression
- cell death
- cell therapy
- endoplasmic reticulum stress
- signaling pathway
- transforming growth factor
- squamous cell carcinoma
- papillary thyroid
- patient reported outcomes
- copy number
- vascular endothelial growth factor
- bone marrow
- current status
- dna methylation