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AIM:To determine the role of p38 MAP kinase signaltransduction pathways in diallyl disulfide (DADS)-inducedG2/M arrest in human gastric cancer MGC803 cells.METHODS:MGC803 cell growth inhibition was measuredby MTT assay.Phase distribution of cell cyde was analyzed byflow cytometry.Expression of Cdc25C,p38,phosphorylationof p38 (pp38) were determined by Western blotting.RESULTS:MTT assay showed that SB203580,a specificp38 MAPK inhibitor blocked DADS-induced growth inhibition.Flow cytometry analysis revealed that treatment of MGC803cells with 30 mg/L DADS increased the percentage of cellsin the G2/M phase from 9.3% to 39.4% (P<0.05),whereasinhibition of p38 activity by SB203580 abolished inductionof G2/M arrest by DADS.Western blotting showed thatphosphorylation of p38 was increased 3.52-fold followingtreatment of MGC803 cells with 30 mg/L DADS for 20 min(P<0.05),whereas Cdc25C was decreased 68% followingtreatment of MGC803 cells with 30 mg/L DADS for 24 h(P<0.05).Decreased Cdc25C protein expression by DADSwas attenuated by SB203580 (P<0.05).CONCLUSION:DADS-induced G2/M arrest of MGC803cells involves activation of p38 MAP kinase pathways.Decreased Cdc25C protein expression by p38 MAPK playeda crucial role in G2/M arrest after treatment with DADS.
AIM: To determine the role of p38 MAP kinase signal transduction pathways in diallyl disulfide (DADS) -induced G2 / M arrest in human gastric cancer MGC803 cells. METHODS: MGC803 cell growth inhibition was measured by MTT assay. Phase distribution of cell cyde was analyzed by flow cytometry .Expression of Cdc25C, p38, phosphorylationof p38 (pp38) were determined by Western blotting.RESULTS: MTT assay showed that SB203580, a specificp38 MAPK inhibitor blocked DADS-induced growth inhibition. Flow cytometry analysis showed that treatment of MGC803 cells with 30 mg / L DADS increased the percentage of cells in the G2 / M phase from 9.3% to 39.4% (P <0.05), while inhibition of p38 activity by SB203580 abolished induction of G2 / M arrest by DADS. Western blotting showed that phosphorylation of p38 was increased 3.52-fold following treatment MGC803 cells with 30 mg / L DADS for 20 min (P <0.05), whereas Cdc25C was decreased 68% following treatment of MGC803 cells with 30 mg / L DADS for 24 h (P <0.05) .Decreased Cdc25C protein expression by DADS was attenuated by SB203580 (P <0.05). CONCLUSION: DADS-induced G2 / M arrest of MGC803 cells involved in activation of p38 MAP kinase pathways. Decreased Cdc25C protein expression by p38 MAPK played crucial roles in G2 / M arrest after treatment with DADS .