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. 2017 Dec 6;8(70):114474–114480. doi: 10.18632/oncotarget.22967

Figure 1.

Figure 1

(A) Loss of function shRNA library screening plotted against the viability of MyLa cell line for each shRNA target. Selected kinases which decreased the viability by 80% (dotted line) are highlighted. MyLa was chosen as a model in this high-throughput screen as GATA-3 confers resistance to chemotherapy in a cell-autonomous manner in these cells, as observed in other cutaneous and peripheral T-cell lympohmas. Three independent experiments were performed and the effect of kinase knockdown on cell viability was determined by MTT assay, and normalized to non-targeting shRNA controls, as described [12]. (B–E) MyLa cells were treated with volasertib at the concentrations indicated; (B) Cell viability was measured by CellTiter Glo reagent assay from Promega Corporation, WI. (C) Apoptosis evaluated by Annexin V/propidium iodide incorporation. (D) Cell viability at 24 and 48 hours measured with CellTiter Glo assay. (E) PARP, caspase 8, and caspase 3 cleavage examined by immunoblotting. (F) Apoptosis following volasertib treatment was examined in two primary T-cell lymphoma samples (TCL1 and TCL2) by Annexin V/PI incorporation.