Figure 1
Schematic diagram illustrating the limitation of mTORC1 inhibitors for anticancer therapy. (A) Anabolic cellular metabolism involving the PI3K-mTORC1 pathway predominantly leads to cancer proliferation, while simultaneously suppressing catabolic cellular metabolism, which is required for cell growth and survival during nutrient starvation. This metabolic balance is finely controlled by mTORC1. (B) When mTORC1 is inhibited by treatment with targeted therapeutics or environmental nutrient deprivation, catabolic processes including macroautophagy and lysosome-dependent degradation of extracellular proteins derived from macropinocytosis are significantly increased to support cancer cell proliferation, ultimately affecting drug efficacy depending on the tumor microenvironment.
