Gemcitabine resistance induced by interaction between alternatively spliced segment of tenascin-C and annexin A2 in pancreatic cancer cells.

Pancreatic cancer is the fourth leading cause of cancer-related death in the western countries and it is resistant to almost all cytotoxic drugs. In the current study, we explored the gemcitabine resistance induced by the interaction between Annexin A2 (ANXA2) and alternatively spliced segment of tenascin-C (TNfnA-D). In the pancreatic cancer cell culture system in vitro, it was proved that exogenous recombinant TNfnA-D combined with the cell surface ANXA2 specifically and their interaction suppressed gemcitabine-induced cytotoxicity on pancreatic cancer cells in a dose-dependent manner.

Blockade of hedgehog signaling pathway as a therapeutic strategy for pancreatic cancer.

Recent studies have demonstrated that pancreatic adenocarcinoma cells require hedgehog (HH) signaling for proliferation and survival. Mutations in the smoothened (SMOH) gene and loss-of-function mutations in the patched (PTCH) gene, which are involved in the HH signaling pathway, may cause pancreatic tumors. Since HH signaling pathway may contribute to the induction and maintenance of pancreatic tumors, the use of HH pathway inhibitors for targeting the pancreatic cancer might represent a novel therapeutic approach to advanced pancreatic carcinoma.