A 1210477

For oxidative stress-induced senescence END-MSCs/WJ-MSCs were treated with 200 µM/100 µM H₂O₂ (Sigma) for 1 h. For doxorubicin-induced senescence DP-MSCs/A549 were treated with 1 μM of doxorubicin (Veropharm) for 3 days. In each case cells were considered senescent not earlier than 14 days after treatment. For replicative senescence AD-MSCs earlier than 4th passage were identified as control cells and later than 10th as senescent ones. For etoposide-induced senescence A549/END-MSCs/SK-Hep1 were treated with 2 µM/5 µM/3 µM etoposide (Veropharm) for 3 days and analyzed not earlier than 7 days after senescence induction. In this case, treatment design completely coincided with those described in the study from which RNA-seq data originated (Wang et al., 2017). Two cardiac glycosides we applied as senolytic compounds—Ouabain (Sigma) and Bufalin (Calbiochem).
In order to compare stress-resistance between control and senescent END-MSCs or A549, cells were treated either with 400/800 µM H₂O₂ (Sigma) for 1 h or with 0.3/1 µM staurosporine (Sigma). Cell viability was analyzed in 48 h after stress induction.
To block MCL-1 activity END-MSCs were pretreated with 10 µM of A-1210477 (Sigma) for 3 days.

Dasatinib (BMS-354825) and trametinib (GSK-1120212) were purchased from LC Laboratories (Woburn, MA, USA); MK2206 and ABT-263 were purchased from Selleckchem (Houston, TX, USA). A-1210477 was purchased from Sigma Aldrich (St. Louis, MO, USA). All drugs were dissolved in dimethyl sulfoxide at 10 mM stocks.