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Background  In a classic model, G i α proteins including G i1 α, G i2 α and G i3 α are important for transducing signals from G i α protein-coupled receptors (G i αPCRs) to their downstream cascades in response to hormones and neurotransmitters. Our previous study has suggested that G i1 α, G i2 α and G i3 α are also important for the activation of the PI3K/Akt/mTORC1 pathway by epidermal growth factor (EGF) and its family members. However, a genetic role of these G i α proteins in the activation of extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) by EGF is largely unknown. Further, it is not clear whether these G i α proteins are also engaged in the activation of both the Akt/mTORC1 and ERK1/2 pathways by other growth factor family members. Additionally, a role of these G i α proteins in breast cancer remains to be elucidated.    Results  We found that Gi1/3 deficient MEFs with the low expression level of G i2 α showed defective ERK1/2 activation by EGFs, IGF-1 and insulin, and Akt and mTORC1 activation by EGFs and FGFs. Gi1/2/3 knockdown breast cancer cells exhibited a similar defect in the activations and a defect in  in vitro  growth and invasion. The G i α proteins associated with RTKs, Gab1, FRS2 and Shp2 in breast cancer cells and their ablation impaired Gab1’s interactions with Shp2 in response to EGF and IGF-1, or with FRS2 and Grb2 in response to bFGF.    Conclusions  G i α proteins differentially regulate the activation of Akt, mTORC1 and ERK1/2 by different families of growth factors. G i α proteins are important for breast cancer cell growth and invasion.

Giα proteins exhibit functional differences in the activation of ERK1/2, Akt and mTORC1 by growth factors in normal and breast cancer cells