Skip to main content
. 2021 Dec 20;17(12):e1009953. doi: 10.1371/journal.pgen.1009953

Fig 2. mTOR allows senescence escape in the presence of an ER stress.

Fig 2

A. Senescent cells were transfected with a control siRNA or a siRNA directed against p21. Cell extracts were analyzed by SWATH quantitative proteomics and GSEA analysis 2 days after p21 depletion (n = 3). B. Analysis of the expression of the UPR markers in LS174T and MCF7 senescent cells after 3 days of emergence (noted E3 on the figure, n = 3). C. Senescent MCF7 and LS174T cells were treated with increasing concentrations of tunicamycin as indicated and the number of emerging clones was evaluated 10 days later (n = 4, Kolmogorov-Smirnov test, * = p<0.05). UPR induction was validated by Western blot 24 hr after the treatment of senescent cells with the lowest concentration of tunicamycin (LS174T: 0.1 μg/ml, n = 2; MCF7:1 μg/ml, n = 2). D. After senescence induction, cells were stimulated with 10% FBS in the presence or absence of mTOR inhibitors. Cell extracts were recovered 7 days later and the expression of Bip was analyzed by western blot (n = 3). E, F. Following senescence induction, cells were transduced with a control shRNA or a shRNA directed against TSC2 (MCF7) or with a control siRNA or a siRNA directed against TSC2 (LS174T cells). TSC2 inhibition was validated by western blot 2 days after transduction (E. LS174T n = 2, MCF7 n = 1). F: Cells were then washed and treated or not with tunicamycin (LS174T: 0.1μg/ml, MCF7 1μg/ml) and emergence was then evaluated as above (n = 4 to 8, Kolmogorov-Smirnov test, * = p<0.05 ** = p<0.01).