RESUMEN
Objective To investigate the expression of transmembrane protein 16 F (TMEM16 F) in breast cancer cells and to elucidate the effect of the knockdown of its gene on proliferation and migration of T47 D breast cancer cells. Methods The expression of TMEM16 F protein in MDA-MB-231 and T47 D breast cancer cells was detected by Western blotting. The effect of TMEM16 F knockdown on the proliferation of T47 D breast cancer cells was detected by CCK-8 cell proliferation assay, and its effect on the migration of T47 D breast cancer cells was examined by cell scratch assay. Results Western blotting results showed TMEM16 F protein expression in breast cancer cells.The results of CCK-8 cell proliferation assay showed that compared to the Scrambled shRNA group, the proliferation of T47 D breast cancer cells was decreased after TMEM16 F knockdown (P = 0.037 0). The results of the scratch test showed that the migration ability of T47 D breast cancer cells was enhanced after TMEM16 F knockdown, compared to the control group (P = 0.002 7). Conclusion TMEM16 F is highly expressed in T47 D breast cancer cells. Knockdown of TMEM16 F can inhibit the proliferation and promote the migration of T47 D breast cancer cells.
RESUMEN
Objective To investigate the effect of channel density on the gating properties of Anoctamin 1(Ano1,TMEM16A)Ca2+?activated chlo?ride channel. Methods Ano1 expression plasmids were transiently transfected into HEK293 cells. High density and low density of Ano1 was ob?tained after expressing the protein for 24 h and 6 h,respectively. Electrophysiological recordings were performed in the whole?cell patch clamp con?figuration. The activation kinetics of current traces was fitted by exponentials. Results The current density was significantly higher in cells express?ing Ano1 for 24 h than those expressing Ano1 for 6 h(P0.05). Conclusion Our findings suggested that chan?nel density regulates the gating of Ano1. High channel density promotes activation of Ano1.
RESUMEN
To study the effect of chitosan on delayed outward potassium current(IK) in single ventricular myocytes of guinea pig and investigate its antiarrhythmic mechanism from ion channel view. Patch clamp technique with whole-cell configuration. Holding potential was -40mV,commanding potential was -60- + 70mV ,step pulse +10mV,stimulating frequency 1 Hz,duration 300 ms and stimulating interval 6s. The result showed that Chitosan inhibited IK in a dose -dependent manner. Conclusion :Chitosan can inhibite IK in single ventricular myocytes of guinea pig.
RESUMEN
AIM To investigate the effect of N methyl berbamine(NMB)on ATP sensitive potassium currents( I KATP )in single ventricular myocytes of guinea pig. METHODS Patch clamp technique with whole cell configuration. Holding potential was -40 mV, commanding potential was -100～+50 mV and duration was 600 ms. Pipette solution contained 0 3 mmol?L -1 ATP. RESULTS NMB inhibited I KATP in a concentration dependent manner. When holding potential was -40 mV and command potential was 0 mV, I KATP were reduced from (0 46?0 09) nA, (0 43?0 15) nA, and(0 47?0 10) nA to (0 37?0 07) nA( n=4,P