Paclitaxel induced cytotoxicity and apoptosis in FLCN-deficient renal cancer cells. A. Cells were treated with 100 nM paclitaxel or a control vehicle, cell viability was measured by MTT assay. Compared with UOK257-2 and ACHN-sc cells, FLCN-deficient UOK257 and ACHN-5968 cells were more sensitive to paclitaxel-mediated cytotoxicity. (*: p < 0.05. UOK257 with Paclitaxel vs UOK257-2 with Paclitaxel; ACHN-sc with Paclitaxel vs ACHN 5968 with Paclitaxel; n = 15) B. Cells were treated with 50, 80, and 100 nM paclitaxel for 24 hours. TUNEL assay was used for apoptosis analysis. FLCN-deficient cells (UOK257 and AHN-5968) showed more cell death compared to FLCN-expressing counterparts. (*: p < 0.05. UOK257 vs UOK257-2; ACHN-sc vs ACHN 5968; n = 15). C. Cells treated with 100 nM Paclitaxel or a control vehicle were stained with DAPI and analyzed under fluorescence microscope. Bright blue fluorescent signals showed the damaged nuclear DNA due to apoptosis. More bright blue fluorescent spots were observed in FLCN-deficient cells. Scale bar = 10 μm. D. Cells were treated with 50, 80, and 100 nM paclitaxel for 24 hours, cleaved caspase-3 and FLCN protein were detected by western blot. Elevated cleaved caspase-3 expression was detected in FLCN-deficient cells.