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Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
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CASK regulates Notch pathway and functions as a tumor promoter in pancreatic cancer

Jun Qu1, Yeqi Zhou2, Yuan Li3

  • 1Department of Emergency Medicine, Nanyang First People's Hospital, Nanyang, 473012, China.

Archives of Biochemistry and Biophysics
|February 6, 2021
PubMed

Insights

Calcium/calmodulin-dependent serine protein kinase (CASK) is upregulated in pancreatic cancer, promoting malignant behaviors. Silencing CASK inhibits tumor growth and metastasis by inactivating the Notch pathway, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling

Background:

  • Calcium/calmodulin-dependent serine protein kinase (CASK) is a MAGUK family member involved in cell proliferation, cytoskeletal remodeling, and metastasis.
  • Understanding CASK's role in pancreatic cancer is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the effect of CASK on pancreatic cancer malignancy.
  • To identify the signaling pathway regulated by CASK in pancreatic cancer.

Main Methods:

  • Analysis of CASK expression in pancreatic cancer tissues using TCGA database and GEPIA.
  • Assessment of overall survival (OS) and disease-free survival (DFS) based on CASK expression.
  • KEGG pathway enrichment analysis to identify CASK-associated pathways.
  • Experimental validation using Western blot, CCK-8, colony formation, Transwell invasion, and flow cytometry assays.

Main Results:

  • CASK expression is upregulated in pancreatic cancer tissues and cells.
  • High CASK expression correlates with shorter OS and DFS in pancreatic cancer patients.
  • CASK and associated genes are significantly linked to the Notch pathway.
  • CASK silencing suppressed proliferation, colony formation, and invasion, while inducing apoptosis in pancreatic cancer cells.
  • CASK knockdown inhibited the Notch pathway, and Notch1 overexpression counteracted CASK knockdown's anti-tumor effects.

Conclusions:

  • CASK promotes malignant behaviors in pancreatic cancer.
  • CASK inactivation of the Notch pathway is responsible for its pro-tumorigenic effects.
  • CASK represents a potential therapeutic target for pancreatic cancer treatment.
Keywords:
ApoptosisCASKGrowthInvasionNotch pathwayPancreatic cancer

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