Crosstalk between ERK, AKT, and cell survival

Cancer Biol Ther. 2014 Mar 1;15(3):245-6. doi: 10.4161/cbt.27541. Epub 2014 Jan 14.


It is historically well known that signaling by the PI3K-AKT and MEK1/2-ERK1/2 pathways in a cell type-dependent fashion can collaborate to maintain cell viability. (1)(-) (3) Signaling pathways can also crosstalk with each other wherein one pathway can signal to either enhance or suppress signaling by another. (4) Signaling by the ERK1/2 pathway can also stimulate release of growth factors which can feed back onto tumor cells to re-energize signaling pathways. (5) The studies described by Toulany et al. add to this knowledge base by examining the relationship between PI3K-AKT and MEK1/2-ERK1/2 pathway signaling, EGF receptor signaling, K-RAS function, and tumor cell survival. (6.)

Keywords: EGFR; HNSCC; K-RAS; MAPK/ERK; NSCLC; PI-103; PI3K/Akt; erlotinib.

Publication types

  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Humans
  • Mitogen-Activated Protein Kinase 1 / metabolism*
  • Oncogene Protein v-akt / metabolism*
  • Phosphoinositide-3 Kinase Inhibitors*
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins / metabolism*


  • KRAS protein, human
  • Phosphoinositide-3 Kinase Inhibitors
  • Proto-Oncogene Proteins
  • Oncogene Protein v-akt
  • MAPK1 protein, human
  • Mitogen-Activated Protein Kinase 1
  • Proto-Oncogene Proteins p21(ras)
  • ras Proteins