Fig. 2.

Induction of apoptosis, pancreatic cancer cell killing and cell viability inhibition by FL118: a and b, FL118 treatment results in activation of caspase-3 and cleavage of PARP. Subconfluent pancreatic cancer cells (A, PANC1; B, MIA PaCa2) were treated with FL118 as shown, and the activation of casepase-3 and cleavage of PARP were detected by western blots. GAPDG is the internal control for total protein loading. c, FL118 induces pancreatic cancer cell death. Subconfluent PANC1 and Mia2 pancreatic cancer cells were treated with vehicle or with FL118 at 10, 10 and 500 nM for 48 h. Then the sub-G1 DNA content (later apoptotic dead cells) was determined by flow cytometry. Relative sub-G1 DNA production levels were analyzed and the data were derived from 3 independent testing and shown as histogram as mean ± SD. d, FL118 inhibits pancreatic cancer cell viability. Subconfluent Mia2, PANC1 and BxPC3 pancreatic cancer cells as well as normal human dermal fibroblast cells were treated with vehicle (no FL118) or with a series of FL118 concentrations as shown for 72 h. Then the cell viability was determined using MTT assay. The data were shown as histogram with mean ± SD derived from 3 independent testing assays