PMC:4197337 / 18621-20212 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/4197337","sourcedb":"PMC","sourceid":"4197337","source_url":"https://www.ncbi.nlm.nih.gov/pmc/4197337","text":"VB promoted apoptosis via p53 in human CRC cells\nBased on the cell proliferation inhibition data, we selected 48-htreatment of CRC HCT-116 and HT-29 as the optimal time frame for apoptosis experiments. We used drug doses of 25, 50, and 100 μM of VB to treat cells for 48 h (Figure 5A, B), and used FITC Annexin-V/PI method to measure apoptosis induced by VB. Our data showed the apoptosis rate to be significantly increased by VB in a dose-dependent manner (Figure 5C). Interestingly, this pro-apoptotic effect by VB was countered by a p53-specific inhibitor, FPT-a (Figure 5D). This suggests that VB promotes apoptosis in CRC cells through ap53-dependent mechanism.\nFigure 5 Verbascoside (VB) promoted apoptosis via p53 in human CRC cells. CRC HCT-116 and HT-29 cells were treated by VB at indicated doses and duration, and then analyzed for apoptosis by flow cytometry. Inhibition at 25, 50, and 100 μM of VB to HCT-116 cells was 20.20 ± 4.08%, 43.28 ± 9.80%, and 56.79 ± 9.11% (A), and HT-29 cells, 4.36 ± 3.39%, 18.22 ± 3.94%, and 37.01 ± 6.98%, respectively (B). HCT-116 apoptosis rate after being treated with 25, 50, and 100 μM of VB was 10.83 ± 1.28%, 11.25 ± 1.54%, and 20.19 ± 2.8%, and the HT-29 apoptosis rate, 18.92 ± 6.12%, 21.57 ± 4.05%, and 25.14 ± 6.73%, respectively (C). HCT-116 and HT-29 apoptosis rate was 11.25 ± 1.54% and 21.57 ± 4.05% after being treated with 50 μM Verbascoside; and 5.03 ± 2.77% and 3.11 ± 1.16% after being treated with FPT-a (p53-specific inhibitor); and 5.02 ± 0.73% and 3.18 ± 1.82% after being treated with FPT-a and 50 μM VB respectively (D).","divisions":[{"label":"title","span":{"begin":0,"end":48}},{"label":"label","span":{"begin":667,"end":675}}],"tracks":[]}