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. 2011 Aug 17;6(8):e23754. doi: 10.1371/journal.pone.0023754

Figure 2. HCT116 PTTG1−/− and SW620 PTTG1 knock down (PTTG1-kd) cells exhibit enhanced drug-induced senescence.

Figure 2

a) HCT116 WT, PTTG1−/− and PTTG1 re-introduced PTTG1−/− (PTTG1−/− +PTTG1) cells were plated in 96-well plates for 24 hours and treated with control vehicle (C) or TSA for another 48 hours. DNA synthesis was assessed by measuring BrdU incorporation; b) HCT116 WT and PTTG1−/− cells were plated for 24 hours and treated with control vehicle (C) or TSA (0.005 uM) for another 48 hours, fixed, stained for β-gal activity and cell number counted; c) SW620 WT, PTTG1 knock down (PTTG1-kd) cells and PTTG1-transfected (PTTG1-tf) cells were plated in 96-well plates for 24 hours and treated with control vehicle (C) or doxorubicin (Dox) for another 48 hours, DNA synthesis was assessed by measuring BrdU incorporation; d) SW620 WT, PTTG1 knock down (PTTG1-kd) cells and PTTG1 transfected (PTTG1-tf) cells were plated in 24-well plates for 24 hours, treated with control vehicle (C) or doxorubicin (0.02 uM) for another 48 hours, β-gal staining performed and positive cells counted. Each experiment was repeated three times. Results are expressed as mean±SD, n = 3, *p<0.05, **p<0.001.