Genistein Inhibits the Proliferation of Human Lung Cancer PC14 Cells through the ERK and JNK Pathways / 中国医科大学学报

Objective To investigate the effect of genistein on the proliferation of human lung cancer PC14 cells and the underlying mechanisms. Methods Cell proliferation was examined using the MTT and colony formation assays. Western blotting was used to analyze protein expression levels. Results Genistein significantly inhibited the proliferation of PC14 cells in a concentration and time dependent manner. PD98059, SB203580, and SP100625, three specific inhibitors of the MAPK pathway, significantly inhibited the proliferation of PC14 cells. Moreover, genistein inhibited the phosphorylation of ERK and JNK in a dose dependent manner. Conclusion Genistein can inhibit the proliferation of PC14 cells, which may be related to its inhibitory effect on ERK and JNK activation.

Sorafenib inhibits the proliferation of human oral cancer TCA8113 cells through the activation of p38MAPK / 实用口腔医学杂志

Objective:To investigate the effect of sorafenib on the proliferation of human oral cancer TCA8113 cells and to explore the underlying mechanisms.Methods:Mter treated with sorafenib at 2.5,5,10,20 μg/ml respectively for48 h,TCA8113 cell proliferation was examined by MTT and colony formation assay.Western blotting was employed to examine the p38MAPK expression in the cells.TCA8113 cells were pretreated with 10 μmol/L of SB203580 (a specific inhibitor of p38MAPK) for 30 min,and then by different concentrations of sorafenib for 48 h,cell proliferation was tested by MTT assay.Results:Sorafenib significantly inhibited the proliferation of TCA8113 cells in a concentration dependent fashion.Sorafenib also remarkably promoted the activation of p38MAPK of the cells.SB203580 significantly alleviated soiafenib induced TCA8113 cell viability decrease.Conclusion:Sorafenib can inhibit the proliferation of TCA8113 cells,which may be related to the activation of p38MAPK.

Genistein inhibits proliferation of human oral cancer TCA8113 cells through suppression of VEGF expression / 中国病理生理杂志

AIM:To investigate the effect of genistein on the proliferation of human oral cancer TCA 8113 cells and to explore the underlying mechanisms .METHODS:The cell proliferation was examined by MTT assay , cell counting and colony formation assay .Western blotting was employed to examine the protein levels of vascular endothelial growth fac -tor (VEGF), extracellular signal-regulated kinase (ERK) and p-ERK.RESULTS: Genistein significantly inhibited the proliferation of TCA8113 cells in a concentration-dependent fashion .Moreover , genistein dose-dependently decreased the protein levels of VEGF, ERK and p-ERK.The expression of VEGF was also blunted by U 0126, a specific inhibitor of ERK.U0126 and axitinib, a VEGF receptor antagonist , both significantly inhibited the proliferation of TCA 8113 cells. CONCLUSION:Genistein inhibits the proliferation of TCA8113 cells, which may be related to its inhibitory effect on ERK expression and activation , thus subsequently decreasing the expression of VEGF .

L-Carnitine inhibits H2 O2-mediated NFATc3 nuclear translocation / 中国病理生理杂志

AIM: To explore the effect of L-carnitine on nuclear factor of activated T-cells, cytoplasmic 3 (NFATc3) in cardiomyocytes under H2O2 stimulation.METHODS: Primary cultured neonatal rat myocardial cells were stimulated by H2 O2 at concentration of 200μmol/L for 12 h to induce oxidative stress injury.In treatment group, L-carni-tine and cyclosporin A ( CsA) , a specific inhibitor of calcineurin ( CaN) , were administered 30 min prior to H2 O2 stimula-tion.After treatment, total, cytoplasmic and nuclear NFATc3 protein levels were determined by Western blotting.The method of immunofluoresence was used to evaluate the distribution of NFATc3.RESULTS: H2 O2 treatment produced no effect on the expression of total NFATc3, but caused its translocation from the cytosolic to nuclear compartment, which was greatly blunted by L-carnitine pretreatment.CONCLUSION:L-carnitine antagonized oxidative stress injury via alleviating NFATc3 nuclear translocation.