“Heat shock protein 70 in pancreatic diseases: Friend or foe” Article Swipe

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Hsp70 Trypsinogen Medicine Apoptosis Pancreatic cancer Pancreatitis Heat shock protein Shock (circulatory) Cancer research Pancreatic injury Acinar cell Internal medicine Cell biology Cancer Trypsin Enzyme Biology Biochemistry Gene

Bhuwan Giri , Vrishketan Sethi , Shrey Modi , Bharti Garg , Sulagna Banerjee , Ashok K. Saluja , Vikas Dudeja ·

YOU? · · 2017 · Open Access · · DOI: https://doi.org/10.1002/jso.24653 · OA: W2620519531

The heat shock response in pancreatitis that is activated via HSP70 protects acinar cells through multiple simultaneous mechanisms. It inhibits trypsinogen activation and modulates NF‐κB signaling to limit acinar cell injury. On the other hand, HSP70 is overexpressed in pancreatic cancer and is hijacked by the cellular machinery to inhibit apoptosis. Inhibition of HSP70 in pancreatic cancer by a novel compound, Minnelide, has shown considerable clinical promise.