RESUMEN
Objective To investigate the effect of dihydromyricetin on proliferation and apoptosis of breast cancer MCF-7 cells.Methods From March 2014 to February 2015,breast cancer MCF-7 cells were treated with 99% pure DMY as an inhibitor.MTT assay,flow cytometry and immunocytochemistry were used to analyze the proliferation,apoptosis and protein expression of breast cancer cell MCF-7.Results When the DMY concentration was higher than 20 μg/mL,the inhibitory effect appeared,but not good.When 40 and 80 μg/mL DMY were used,the proliferation of MCF-6 cells were significantly inhibited,and have different degrees of sensitivity to it.When DMY was 80 μg/mL,the IC50 was 226.9 μg/mL.The inhibition rate and IC50 were compared with 0 μg/mL DMY,there was significant difference(P 50%,especially in DMY with 80 μg/mL,the positive rate was 10.00%.Compared with 0 μg/mL DMY,the difference was significant(P<0.05).Conclusion The use of dihydromyricetin in breast cancer patients can effectively inhibit the rapid increase of cancer cells,accelerate apoptosis,slow down the patient′s condition,the effect is outstanding.
RESUMEN
Objective: To investigate the effect of D-α-tocopherol polyethylene glycol 1000 succinate (TPGS) on the inhibition of proliferation of breast cancer cells MCF-7 by baohuoside I. Methods: The cytotoxicity of baohuoside I to MCF-7 cells was determined by MTT assay, the cellular uptake of baohuoside I was detected by fluorescence microscopy, and the intracellular baohuoside I was determined by HPLC. Results: The effect of baohuoside I on the inhibition of MCF-7 cell proliferation was enhanced in the presence of TPGS, especially on lower concentration. The uptake rates of MCF-7 within 2 h were 29.51%, 38.12%, and 40.37%, when the proportions of baohuosaide I and TPGS were 1:1, 1:2, and 1:4, respectively. The ratios were increased by 27.92%, 65.24%, and 74.99% compared with those using baohuoside I only. Conclusion: TPGS can increase the uptake rate of baohuoside I in MCF-7 cells and enhance the inhibition of MCF-7 cell proliferation.
RESUMEN
Objective: To study the effects of estradiol plus testosterone on the proliferation and apoptosis of breast cancer cell line MCF-7, and to elucidate the possible mechanism. Methods: The growth of MCF-7 cells treated with estradiol (10-10 mol/L) or testosterone (10-5, 10 -7, 10-9 and 10-11 mol/L) alone or in combination for 24, 48 and 72 h was detected by MTT assay. The cell cycle distribution and the apoptosis rate of MCF-7 cells were determined by flow cytometry (FCM). The expression levels of cyclinD1 and androgen receptor (AR) proteins were examined by FCM. Results: The proliferation ability of MCF-7 cells was elevated after treatment with estradiol, and this effect could be inhibited by a higher concentration of testosterone (10-5 mol/L) while improved by a lower concentration of testosterone (10-9 mol/L). After treatment with estradiol plus testosterone (10-5 mol/L) for 48 h, the G1/S phase transition of MCF-7 cells was accelerated, and the apoptosis rate was increased; the expression level of cyclinD1 protein was increased while no change of AR protein expression was observed. Conclusion: Estradiol combined with testosterone of high concentration can inhibit the proliferation of MCF-7 cells and improve the apoptosis. This effect may be associated with the up-regulation of cyclinD1 expression. Copyright© 2011 by the Editorial Board of Tumor.
RESUMEN
Objective: To investigate the effects of fucoidan on proliferation and apoptosis of breast carcinoma cell line MCF-7 and the underlying mechanism. Methods: Cell viability was measured by MTF assay. Apoptosis was detected by Hoechst 33258 staining and agarose gel electrophoresis. The mRNA and protein expression of bcl-2 and bax were examined by RT-PCR and Western blotting, respectively. Results: Fucoidan effectively inhibited the proliferation of MCF-7 cells in a concentration-dependent manner (P <0.01). Fucoidan induced significant apoptosis of MCF-7 cells characterized by fragmented DNA ladder. Fucoidan down-regulated the expression of bcl-2 and up-regulated bax at mRNA and protein levels. The ratio of bcl-2 to bax decreased with the increase in the fucoidan concentrations (P < 0.05). Conclusion: Fucoidan inhibites the proliferation and induced the apoptosis of MCF-7 cells. The underlying mechanism may be related with down-regulation of anti-apoptotic protein bcl-2 and up-regulation of apoptotic protein bax.
RESUMEN
Objective: To elucidate effects of mammalian sterile 20-like kinase 1 (MST1) gene on cell proliferation and apoptosis of human breast carcinoma cell line MCF-7. Methods: This study constructed plasmid pCMV-FLAG-MST1 and transfected it into human breast carcinoma cell line MCF-7 via mediation by Lipofectamine 2000. We detected the efficiency of transfection by Western blotting. The effect of MST1 on cell proliferation was measured by MTT assay at 12, 24, 36, and 48 h after transfection. The effect of MST1 on cell proliferation was also determined by BrdU incorporation assay at 36 h after transfection. Cisplatin was added into cultured cells at 36 h to induce apoptosis. Forteen hours later cell apoptosis was detected by Annexin V staining. Results: This study successfully constructed plasmid pCMV-FLAG-MST1. The MTT and BrdU incorporation assay showed that the cell proliferation was significantly inhibited after transfection of pCMV-FLAG-MST1. Annexin V staining demonstrated that cell apoptotic rate was relatively higher after overexpression of MST1. Conclusion: In summary, overexpression of MST1 decreases cell proliferation and induced apoptosis of human breast carcinoma cell line MCF-7.
RESUMEN
0.05),the inhibitory rates in the other groups were increased compared with control group(P0.05),the expressions of COX-2 and VEGF in MCF-7 cells in the other groups were lower than that in negative control group(P
RESUMEN
OBJECTIVE: To study the in vitro anti-tumor activity of tungstophosphate compound(K6[P2W18O62]?14H2O) with Dawson structure.METHODS: MCF-7 cells were treated with different concentration of K6[P2W18O62]?14H2O,then its IC50 was measured by MTT assay;flow cytometry was applied to analyze cell cycle and apoptosis by computing the ratio of MCF-7 cells in different phase and its apoptotic ratio.Cell growth and viability were measured by trypan blue staining and cell counting by computing the ratio of living cells.The synergetic anti-tumor activity of tungstophosphate compound(K6[P2W18O62]?14H2O) and pharmorubicin was studied.RESULTS: K6[P2W18O62]?14H2O inhibited MCF-7 cell proliferation with IC50 of(33.7?3.2) ?mol?L-1,it reduced the proportions of MCF-7 cells at S phase and G1 phase,with the apoptotic rate at 3.7%～29.2% within 48 h.The percentage of living cells was 95.37%～76.78% at 48 h.As compared with pharmorubicin alone,the addition of K6[P2W18O62]?14H2O to pharmorubicin showed a significantly higher inhibitory action on proliferation of MCF-7 cells(P