Article Figures & Data
Figures
- Figure 1.
Rapamycin efficacy on HCT-116 cells and Hs-27 cells in vitro. Cell viability was measured with the WST-8 reagent. The concentration axis uses a log2 scale. IC50: Half-maximal inhibitory concentration.
- Figure 2.
Recombinant methioninase (rMETase) efficacy on HCT-116 cells and Hs-27 cells in vitro. Cell viability was measured with the WST-8 reagent. The concentration axis uses a log2 scale. IC50: Half-maximal inhibitory concentration.
- Figure 3.
Treatment of Hs-27 cells in vitro with recombinant methioninase (rMETase) and rapamycin at their half-maximal inhibitory concentrations (0.96 U/ml and 0.37 nM, respectively) alone and in combination. The combination treatment did not synergistically affect the viability of Hs-27 cells more than either drug alone. Cell viability was measured with the WST-8 reagent. ****p<0.0001.
- Figure 4.
Treatment of HCT-116 cells in vitro with recombinant methioninase (rMETase) and rapamycin at their half-maximal inhibitory concentrations (0.39 U/ml and 1.38 nM, respectively) alone and in combination. The combination treatment significantly reduced the viability of cancer cells. Cell viability was measured with the WST-8 reagent. ****p<0.0001, *p=0.0131.
- Figure 5.
Model showing how rMETase indirectly inhibits mTOR activity by acute depletion of methionine (MET) and SAM in cancer cells resulting in SAMTOR binding to GATOR, thereby inihibiting mTOR.
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