Fig. 2: Modulation of mTORC1 by MCL1 is independent of apoptosis and is mediated by Sestrin 2-TSC2 signaling.
From: MCL1 modulates mTORC1 signaling to promote bioenergetics and tumorigenesis
A Immunoblotting of lysate derived from CHL-1 cells transduced with the indicated shRNAs for 72 h showing that TSC2 knockdown rescues mTORC1 signaling activity in MCL1-depleted cells. The samples derived from the same experiment but different gels for pS6, MCL1, another for TSC2, pS6K1, S6 and another for S6K1 were processed in parallel. B–D Immunoblotting of lysate derived from CHL-1 (B), SK-MEL30 (C), MeWo, IGR1 and IPC298 (D) cells transduced with the indicated shRNAs for 72 h showing an increase in Sestrin 2 protein level in MCL1-depleted cells. The samples derived from the same experiment but different gels for Sestrin2, pS6, another for pS6K1, MCL1, Bcl-xL, another for Sestrin3, S6, Bcl-2 and another for S6K1 were processed in parallel. E Immunoblotting of lysate derived from CHL-1 cells transduced with the indicated shRNAs for 72 h showing that Sestrin 2 knockdown rescues mTORC1 signaling activity in MCL1-depleted cells. F Schematic representation of the model of mTORC1 modulation by MCL1 in melanoma cells. (Created in BioRender. Elgendy, M. (2025) https://BioRender.com/8hqhd6t).
