Contradictory Effect of Notch1 and Notch2 on Phosphatase and Tensin Homolog and its Influence on Glioblastoma Angiogenesis

Authors

  • Mostafa Shabani 1. Medical Genomics Research Center, Tehran Medical Sciences Islamic Azad University, Tehran, Iran 
 2. Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
  • Hamid Taghvaei Javanshir 1. Medical Genomics Research Center, Tehran Medical Sciences Islamic Azad University, Tehran, Iran 
 2. Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
  • Ahmad Bereimipour 2. Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran 
 3. Young Researchers and Elite Club, Tehran Medical Sciences Islamic Azad University, Tehran, Iran
  • Amin Ebrahimi Sadrabadi 2. Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
  • Arsalan Jalili 2. Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
  • Karim Nayernia 4. International Center for Personalized Medicine, Düsseldorf, Germany

DOI:

https://doi.org/10.31661/gmj.v10i.2091

Keywords:

Glioblastoma; Angiogenesis; Notch1; Notch2

Abstract

Many genes induce angiogenesis in tumors, and among them, Notch family genes have received particular attention due to their extensive network of connections with other genes active in this function. Suppression of angiogenic signaling has been studied in various cancers, confirming Notch's fundamental and extensive role. According to studies, four Notch genes work independently with many genes such as vascular endothelial growth factor, phosphatase and tensin homolog, Phosphoinositide 3-kinase/Akt, and matrix metalloproteinases, and so many other genes, as well as proteins (such as hypoxia-inducible factor-1 alpha) significantly affect tumor angiogenesis. Notch1 regular activity in a healthy person causes angiogenesis in body tissues, controlled by normal Notch2 activity. However, in many cases of glioblastoma, whether on patients or tumor xenografts or in vivo models, a mutation in one of these two essential genes or at least one of the genes and proteins that affected by them can cause better angiogenesis in hypoxic conditions and lead to become an invasive tumor. In this review, we examined the contrasting activity of Notch1 and Notch2 and the signaling cascade that each generates in the angiogenesis of glioblastoma, the most invasive cancer of the central nervous system. [GMJ.2021;10:e2091]

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Published

2021-10-05

How to Cite

Shabani, M., Taghvaei Javanshir, H., Bereimipour, A., Ebrahimi Sadrabadi, A., Jalili, A., & Nayernia, K. (2021). Contradictory Effect of Notch1 and Notch2 on Phosphatase and Tensin Homolog and its Influence on Glioblastoma Angiogenesis: . Galen Medical Journal, 10, e2091. https://doi.org/10.31661/gmj.v10i.2091

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Review Article