Effect of isoverbascoside, a phenylpropanoid glycoside antioxidant, on proliferation and differentiation of human gastric cancer cell.
Abstract
AIM: To investigate the effects of phenylpropanoid glycoside antioxidant
isoverbascoside on cell proliferation and differentiation of human gastric cancer
cell line MGC 803.
METHODS: MGC 803 cells were treated with isoverbascoside. Its effects on cell
proliferation, tumorigenicity, enzymatic activities, cell cycles, and gene
expression were respectively evaluated with cell counting, tumor formation assay,
enzymatic assay, flow cytometer analysis, and Western blotting, with Me2SO as
positive control.
RESULTS: Isoverbascoside could markedly inhibit cell proliferation in dose- and
time-dependent manner. Isoverbascoside 20 micromol/L strikingly suppressed cell
tumorigenicity, activities of alkaline phosphatase (ALP), and lactate
dehydrogenase (LDH), and caused G0/G1 arrest. The expression of G1 S checkpoint
related proteins, p53, p21/WAF1, and p16/INK4, were up-regulated after MGC 803
cells were treated with isoverbascoside 20 micromol/L for 4-8 h. Contrarily, the
expression of C-myc protein was suppressed after 8 h treatment.
CONCLUSION: Isoverbascoside inhibited cell proliferation, reversed cell malignant
phenotypic characteristics, and consequently caused differentiation in MGC 803
cells. These effects might be associated with its activities of causing G0/G1
arrest and regulating the expression of cell cycle related proteins.
Keywords:
isoverbascoside on cell proliferation and differentiation of human gastric cancer
cell line MGC 803.
METHODS: MGC 803 cells were treated with isoverbascoside. Its effects on cell
proliferation, tumorigenicity, enzymatic activities, cell cycles, and gene
expression were respectively evaluated with cell counting, tumor formation assay,
enzymatic assay, flow cytometer analysis, and Western blotting, with Me2SO as
positive control.
RESULTS: Isoverbascoside could markedly inhibit cell proliferation in dose- and
time-dependent manner. Isoverbascoside 20 micromol/L strikingly suppressed cell
tumorigenicity, activities of alkaline phosphatase (ALP), and lactate
dehydrogenase (LDH), and caused G0/G1 arrest. The expression of G1 S checkpoint
related proteins, p53, p21/WAF1, and p16/INK4, were up-regulated after MGC 803
cells were treated with isoverbascoside 20 micromol/L for 4-8 h. Contrarily, the
expression of C-myc protein was suppressed after 8 h treatment.
CONCLUSION: Isoverbascoside inhibited cell proliferation, reversed cell malignant
phenotypic characteristics, and consequently caused differentiation in MGC 803
cells. These effects might be associated with its activities of causing G0/G1
arrest and regulating the expression of cell cycle related proteins.