Src kinase in glioblastoma news from an old acquaintance

Claudia Cirotti, Claudia Contadini, Daniela Barilà

Research output: Contribution to journalReview articlepeer-review


Glioblastoma multiforme (GBM) is one of the most recalcitrant brain tumors characterized by a tumor microenvironment (TME) that strongly supports GBM growth, aggressiveness, invasiveness, and resistance to therapy. Importantly, a common feature of GBM is the aberrant activation of receptor tyrosine kinases (RTKs) and of their downstream signaling cascade, including the non-receptor tyrosine kinase SRC. SRC is a central downstream intermediate of many RTKs, which triggers the phosphorylation of many substrates, therefore, promoting the regulation of a wide range of different pathways involved in cell survival, adhesion, proliferation, motility, and angiogenesis. In addition to the aforementioned pathways, SRC constitutive activity promotes and sustains inflammation and metabolic reprogramming concurring with TME development, therefore, actively sustaining tumor growth. Here, we aim to provide an updated picture of the molecular pathways that link SRC to these events in GBM. In addition, SRC targeting strategies are discussed in order to highlight strengths and weaknesses of SRC inhibitors in GBM management, focusing our attention on their potentialities in combination with conventional therapeutic approaches (i.e., temozolomide) to ameliorate therapy effectiveness.

Original languageEnglish
Article number1558
Pages (from-to)1-21
Number of pages21
Issue number6
Publication statusPublished - Jun 2020


  • Cancer therapy
  • Glioblastoma
  • Inflammation
  • Kinase inhibitor
  • Metabolic reprogramming
  • Receptor tyrosine kinase
  • SRC kinase
  • Therapy resistance
  • Tumor microenvironment

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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