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Cripto-1 overexpression in U87 glioblastoma cells activates MAPK, focal adhesion and ErbB pathways

Faisal Alowaidi1, Saeed M Hashimi2, Naif Alqurashi2

  • 1Department of Pathology and Laboratory Medicine, College of Medicine and University Hospital, King Saud University, Riyadh 11461, Saudi Arabia.

Oncology Letters
|August 28, 2019
PubMed

Insights

Cripto-1 overexpression significantly impacts glioblastoma (GBM) cell function by activating key signaling pathways like MAPK, focal adhesion, and ErbB. This research illuminates Cripto-1

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Signaling

Background:

  • Understanding cancer cell signaling pathways is critical for developing effective cancer therapies.
  • Glioblastoma (GBM) is an aggressive brain tumor with complex underlying molecular mechanisms.
  • Cripto-1 is a protein implicated in various cellular processes, including cancer development.

Purpose of the Study:

  • To investigate the specific effects of Cripto-1 on signaling pathways that regulate glioblastoma (GBM) cell function.
  • To identify the key phosphorylated proteins and pathways influenced by Cripto-1 overexpression in GBM cells.

Main Methods:

  • Overexpression of Cripto-1 in glioblastoma cells.
  • Analysis of protein phosphorylation changes using Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
  • Identification of protein functions using the Uniprot resource.

Main Results:

  • Cripto-1 overexpression significantly impacts multiple signaling pathways, including MAPK (35% proteins phosphorylated), focal adhesion (FA) (27%), and ErbB (24%).
  • Cripto-1 regulates GBM cell proliferation and survival via pathways involving EGFR, FGFR1, Src, FAK, p130CAS, c-Jun, Paxillin, and BCL2.
  • Cripto-1 influences cellular motility and invasion through the FA and ErbB pathways, potentially involving EGFR, Her2, Src, and FAK.

Conclusions:

  • Cripto-1 plays a crucial role in controlling diverse cellular mechanisms within glioblastoma cells.
  • The identified signaling pathways (MAPK, FA, ErbB) provide potential therapeutic targets for GBM treatment.
  • Further research into Cripto-1's regulatory functions can enhance our understanding of GBM biology and treatment strategies.
Keywords:
Cripto-1ErbBMAPKfocal adhesionglioblastomaphosphoproteomesignalling pathways

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