Fig. 1

Schematic illustration of the AMPK/mTOR signaling pathway in TNBC tumor growth and progression. mTORC1 comprises mTOR, mammalian lethal with sec-13 protein 8 (mLST8), and regulatory-associated protein of mammalian target of rapamycin (RAPTOR). mTORC1 is activated by growth factors, nutrients (amino acids), and cellular energy. It stimulates anabolic processes, including protein and nucleotide synthesis via ribosomal protein S6 kinase (S6K), eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1), and hinders catabolic processes, such as autophagy, through Unc-51-like kinase 1 (ULK1). mTORC2 consists of mTOR, mLST8, mammalian stress-activated map kinase-interacting protein 1 (mSIN1), and rapamycin-insensitive companion of mTOR (RICTOR) and is activated by growth factors. mTORC2 activates the AGC kinase family members Akt, serum/glucocorticoid-regulated kinase (SGK), and protein kinase C (PKC). mTORC1 and mTORC2 are commonly activated in human cancers. AMPK activation inhibits mTORC1; however, the effect on mTORC2/Akt is not completely clear. Moreover, AMPK activation represses expression of EGFR, cyclin D1, and cyclin E and phosphorylation of MAPK, Src, and STAT3