Article Figures & Data
Figures
- Figure 1.
UA augmented apoptosis induced by rhTRAIL in TNBCs. TNBC cells treated with UA with and without 100 ng/ml rhTRAIL over a 72-h period. (A) The displayed plots obtained from FACS analysis, Annexin V−/PI+-dead cells are depicted in the left top quadrants, Annexin V−/PI−-viable cells are depicted in the left bottom quadrants, Annexin V+/PI−-early apoptotic cells are depicted in the right bottom quadrants, and Annexin V+/PI+-late apoptotic, dead cells are depicted in the right top quadrants. Bar graphs (B) BT-20 and (C) HCC1937 illustrate the mean total percentage of apoptotic cells (Annexin V+ cells)±SEM derived from three independent experiments performed in triplicate (n=9). * represents p<0.05.
- Figure 2.
UA and rhTRAIL facilitate apoptosis by the extrinsic pathway. Co-treated TNBC (A) BT-20 and (B) HCC1937 cells were sensitized to rhTRAIL-induced apoptosis, as demonstrated by caspase 8 activation, caspase 3 activation, and PARP cleavage.
- Figure 3.
UA-treated cells' expression of DR4 and DR5. Protein levels of DR4 and DR5 (mature form) were determined in (A) BT-20 cells and (B) HCC1937; UA boosted DR4 and DR5 expression in TNBCs following 72 h of treatment in a dose-dependent manner. (C) Protein levels of DR4 and DR5 (mature form) were examined in UA-treated MCF-10A cells, and expression of DRs was not changed. Flow cytometry analysis of cell surface expression of DR4 and DR5 in (D) BT-20 and (E) HCC1937 cells treated with UA; the bar graphs illustrate the mean fold increase in the cell surface expressions of DR4 or DR5 relative to the vehicle-treated control ±SEM from three independent experiments performed in triplicate (n=9). * represents p<0.05.
- Figure 4.
UA transcriptionally controls c-FLIPL down-regulation and DRs up-regulation. (A) Western blot analysis showing that UA decreased the expression of c-FLIPL in TNBC cells in a dose-dependent manner. (B) RT-PCR was executed with β-actin as a positive control in UA-treated (72 h) BT-20 and HCC1937 cells. UA diminished c-FLIPL mRNA expression in TNBC cells and boosted DR4 and DR5 mRNA expression in TNBC cells.
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