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

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

Research output: Contribution to journalReview article

6 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)114-122
Number of pages9
JournalJournal of Surgical Oncology
Volume116
Issue number1
DOIs
StatePublished - Jul 1 2017

Keywords

  • HSP70
  • calcium
  • lysosomes
  • minnelide
  • pancreatic cancer
  • pancreatitis
  • triptolide

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  • Cite this

    Giri, B., Sethi, V., Modi, S., Garg, B., Banerjee, S., Saluja, A., & Dudeja, V. (2017). “Heat shock protein 70 in pancreatic diseases: Friend or foe”. Journal of Surgical Oncology, 116(1), 114-122. https://doi.org/10.1002/jso.24653