Phosphatidylinositol 3-kinase (PI3K) protein kinase B (AKT)/mammalian target of rapamycin (mTOR), PI3K/AKT/mTOR, and mitogen-activated protein kinase (MAPK) signaling pathway activation in gastric cancer (GC)

Phosphatidylinositol 3-kinase (PI3K) protein kinase B (AKT)/mammalian target of rapamycin (mTOR), PI3K/AKT/mTOR, and mitogen-activated protein kinase (MAPK) signaling pathway activation in gastric cancer (GC). Environmental factors, growth factors, genetic mutations, and infections with Helicobacter pylori and Epstein–Barr virus (EBV) activate both PI3K/AKT/mTOR and MAPK signaling pathways via receptor tyrosine kinases (RTKs). Further, PI3K is activated by phosphorylation, inducing the activation of AKT and downstream activation of other protein kinases such as the mammalian target of rapamycin (mTOR). In a similar manner, MAPK cascade is activated, and together with PI3K/AKT/mTOR, contributes to GC development, sustaining growth, survival, proliferation, angiogenesis, and metastasis. In clinical studies, several inhibitors of these protein kinases have been used. Therefore, PI3K, AKT, mTOR, MAPK kinase (MAPKK or MEK1/2), and human epithelial growth receptor 2 (HER2), showed different responses regarding the survival rate. Note: + denotes activation; − denotes inhibition

Publication

Targeting PI3K/AKT/mTOR and MAPK Signaling Pathways in Gastric Cancer (2024) Diana-Theodora Morgos, et al. Int J Mol Sci. 2024 Feb;25(3). Figure: F2. Homo sapiens

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