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Stress-activated kinases as therapeutic targets in pancreatic cancer

Benno Traub1, Aileen Roth1, Marko Kornmann1

  • 1Department of General and Visceral Surgery, Ulm University Hospital, Ulm 89081, Germany.

World Journal of Gastroenterology
|September 9, 2021
PubMed

Insights

Targeting stress-activated protein kinases like c-Jun N-terminal kinases (JNK), p38, and casein kinase 1 (CK1) shows promise for pancreatic cancer. Further research is needed to advance these findings into clinical treatments for improved patient survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Pancreatic cancer has a high incidence and poor survival rates, necessitating novel therapeutic strategies.
  • Protein kinases, including c-Jun N-terminal kinases (JNK), p38, and casein kinase 1 (CK1) family, regulate cellular processes and are implicated in cancer.
  • Dysregulation of these stress-activated protein kinase pathways is observed in various cancers, including pancreatic cancer.

Purpose of the Study:

  • To explore the potential of targeting JNK, p38, and CK1 protein kinases as a therapeutic approach for pancreatic cancer.
  • To review recent advancements in small molecule inhibitors and combination therapies for stress-activated protein kinases.
  • To assess the relevance of these kinase pathways in precision medicine for pancreatic cancer patients.

Main Methods:

  • Review of existing literature on protein kinase inhibitors and their application in cancer therapy.
  • Analysis of *in vitro* results demonstrating the efficacy of targeting JNK, p38, and CK1.
  • Discussion of the role of stress-activated protein kinases in cellular stress responses and cancer development.

Main Results:

  • Recent improvements in small molecule inhibitors have shown promising *in vitro* results against stress-activated protein kinases.
  • Targeting JNK, p38, and CK1 may be particularly relevant for precision medicine in pancreatic cancer.
  • Earlier therapeutic attempts were limited by specificity and off-target effects.

Conclusions:

  • Inhibition of JNK, p38, and CK1 represents a potential therapeutic avenue for pancreatic cancer, especially in precision medicine.
  • Further *in vivo* investigations and clinical trials are essential to translate these findings into effective treatments.
  • Advancing the inhibition of stress-activated kinases requires continued research and development for translational medicine.
Keywords:
Casein kinase 1Mitogen-activated protein kinasesPancreatic cancerSmall molecule inhibitorStress-activated protein kinasesc-Jun N-terminal kinases

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