Oral squamous cell carcinoma is associated with decreased bcl-2/bax expression ratio and increased apoptosis
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Objective: To study the influence of traditional chinese compound recipe changjining decotion on the apoptosis of human large intestine cancer cells and the expression of bcl-2 、bax concerned with the apoptosis . Methods: The sensitivity of Changjining to the large intestine cancer was detected by MTT method. The influence of Changjining decotion on the apoptosis and the expression of bcl-2 and bax was detected by FCM. Results:Changjining had the function of restraining the multiplication of large intestine cancer HT-29 ;The results of FCM indicated that Changjining had the function of promoting the apoptosis and depressing the expression of bcl-2 and bax concerned with the apoptosis ,especially on bcl-2. Conlusions:Changjining has the anticarcinogenic function ,and the mechanisms of which are to improve the apoptosis of cells and to depress the expression of bcl-2 and bax.
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Objective To investigate the apoptosis-inducing effect of arsenic trioxide (As2O3) on human nasopharyngeal carcinoma and its possible mechanism.Methods CNE1cell line was treated with As2O3 at different concentration. Cell apoptosis was evaluated by flow cytometry, transmission electron micros- copy and TUNEL methods. The effect of As2O3on the expression of p53, bax and bcl-2genes was stud- ied with immunohistochemology.Results CNE1cell apoptosis induced by As2O3was detected by FCM, electron microscopy and TUNEL.Typical subdiploid peak before G0/G1phase was observed by flow cy- tometric analysis, showing a dose-and time-dependent effect. Morphological feature of apoptosis, inclu- ding cell shrinkage, nuclear condensation, DNA fragmentation and formation of apoptotic bodies were found under electron microscopy. After48h exposure to As2O3at dose of0.5mg/L,1.0mg/L and 2.0mg/L apoptosis index (AI) accounted by TUNEL staining were2.66±0.64,8.15±0.96and11.59 ±0.68, respectively, which were significantly higher than that of control (0.43±0.43,P0.05). The expression of p53, bax protein was increased sharply in CNE1cell treated with As2O3. Significant posi- tive correction existed between AI and p53protein expression (r=0.554,P=0.011), AI and bax protein expression (r=0.891,P=0.000…). There was positive correction between p53and bax protein expres- sion (r=0.626,P=0.003).Conclusion Arsenic trioxide can induce CNE1cell apoptosis, which was as- sociated with up-regulation of bax and wild-type p53genes expression.
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OBJECTIVE To investigate the protective effect of mogroside on exogenous oxidant induced apoptosis in PC12 cell.METHODS PC12 cells were pre treated with 0.1 and 1 μg·mL-1 mogroside,respectively,followed by 1 h of 400 μM H2O2 incubation.After incubation,cell apoptosis rate was determined by flow cytometry,moreover,Bcl-2 and Bax protein levels were detected by western blot method.RESULTS Apoptosis rate risen by H2O2 was alleviated by pre-incubate with mogroside at 0.1 and 1 μg·mL-1(P0.001).Furthermore,Bcl-2 protein expression was increased,while Bax expression was decreased as well as Bax/Bcl-2 ratio(P0.001).CONCLUSION Mogroside demonstrated protective effect on PC12 cell against H2O2 induced apoptosis,which might be mediated via Bcl-2 family of apoptosis regulatory proteins regulation.
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Objective To study the effect of alcohol on apoptosis and apoptosis-associated genes-Bcl-2 and Bax of cardiac muscle cell.Methods We established an animal experimental model by giving different concentration of alcohol to the healthy mice.Myocardial apoptosis and the expression of apoptosis-associated gene Bcl-2 and Bax were quantitatively analysed by the nuclear fast red-crystal violet staining and immunohistochemical method.Results Some nuclears of the experimental groups were stained purple and agglutinated.Counting under the high power microscope,it was found that the amount of abnormal nuclears significantly increased in alcohol-treated groups compared with the control group (P0.01).Compared with the control,the expression of Bcl-2 in all experimental groups was down-regulated (P0.01) and the granules were stained weak and maldistribution.In contrast,the expression of Bax was up-regulated (P0.01) and the granules engrained and gross.Conclusion The apoptosis of myocardial cells will play an important role in the damage of cardiac muscle induced by alcohol.The myocardial apoptosis caused by alcohol is related to the abnormal expression of apoptosis-associated gene Bcl-2 and Bax.
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Objective The study is to investigate the dynamic expression of Bcl 2 and Bax protein in the apoptosis of primary cultured rat cortical neurons following hypoxia/reoxygenation(H/R)and its relation with apoptosis. Methods The cortical neurons of E16 17 days fetal rat was primarily cultured.The apoptosis model of primary cultured cortical neurons following H/R was established by using TUNEL staining and flow cytometry.The dynamic expression of Bcl 2 and Bax protein at different H/R time was investigated with immunohistochemical method. Results 1.H/R can cause apoptosis of primary cultured rat cortical neurons.In the experiment of H 2R 0,H 4R 0,H 6R 0,H\-8R\-0 and H 2R 18 ,H 4R 18 ,H 6R 18 ,H 8R 18 ,the apoptosis cells occurred after 4 hour hypoxia.The apoptosis cell increased with the time,and reaching peak value at H 8H 18 .2.In the experiment of solo hypoxia group,the expression of Bcl 2 protein decreased with hypoxia time,but Bax increased.They showed obviously negative correlationship.Furthermore,the rate of apoptotic cell also showed obviously negative correlation with Bcl 2 and positive correlation with Bax.However,in hypoxia/reoxygenation group,no correlation was found. Conclusion The apoptosis of primary cultured rat cortical neurons could be induced by H/R.That hypoxia causes the increase of the expression of Bcl 2 protein and the decrease of the expression of Bax protein could be one of the mechanisms of apoptosis.
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Objective:To investigate the mechanism of apoptosis inducing effect of specific COX-2 inhibitor SC236 in gastric cancer cell line SGC7901. Methods: The expression level of apoptosis-regulating proteins Bcl-2,Bak,Bax and CED-9 was analyzed by Western blot method.Cell apoptosis index was measured by fluorescence microscopy as well as by flow cytometry. Results: Treatment of SGC7901 gastric cancer cells with SC236 caused a significant elevation of the expression of the apoptosis-promoting proteins Bak and Bax,but a significant reduction of the expression of the apoptosis-inhibiting protein Bcl-2 and CED-9 were observed.Cell apoptosis index or rate increased with the increment of SC236 concentration and the time of action. Conclusion: Specific COX-2 inhibitor SC236 could induce apoptosis in gastric cancer cell line SGC7901 through the up-regulation of the apoptosis-promoting proteins Bak and Bax,and the down-regulation of the apoptosis-inhibiting protein Bcl-2 and CED-9.
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The amount of bcl-2 mRNA and Bax oncoprotein is increased obviously and the apoptosis and proliferation are active in the lung cancer. Bcl-2 and Bax, especially the ratio of bcl-2 and Bax play an important role in the apoptosis in the lung cancer. The expression of bcl-2 can prevent apoptosis while the expression of Bax induces apoptosis. bcl-2, Bax, apoptosis and PCNA can be used in the lung cancer molecular markers.
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Objective To investigate the apoptosis in endometrial carcinoma cells induced by As_2O_3, and the expression of bcl-2 and bax. Methods In vitro experiments, TUNEL staining method was used to quantitatively and qualitively detect the apoptosis status of endometrial carcinoma cells HEC-1A before and after the As_2O_3 treatment. Immunohistochemical staining was used to detect the expression of apoptosis-regulated gene bcl-2 and bax. Results As_2O_3 was able to induce the apoptosis in endometrial carcinoma cells. As_2O_3 can reduce the expression of apoptosis-regulated gene bcl-2, and up-regulate the expression of apoptosis-regulated gene bax.Conclusions As_2O_3 was able to induce the apoptosis in endometrial carcinoma cells. This apoptosis may be mediated by down-regulation of apoptosis-regulated gene bcl-2 and up-regulation of bax.
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To investigate the effect of icaritin on the proliferation and apoptosis of THP-1 cells and its mechanism.After treated with various concentrations of icaritin, cell proliferation was detected by MTS method, and apoptosis was measured with flow cytometry and Hoechst 33258 staining. Expression of BCL-2, BAX and Caspase-3 protein in THP-1 cell was detected by Western blot.After treatment with various concentrations (4-32 µmol/L) of icaritin for 24, 48, 72 h, the inhibition rate of cell growth significantly increased (P<0.05) in time-dose dependent manner(r=0.946); and the apoptotic rate of cells significantly increased (P<0.05) in time-dose dependent manner(r= 0.924). The expression of BCL-2 protein at 48 h decreased significantly in icaritin-treated group, compared with that in control group (P<0.05), while the expression of BAX and Caspase3 protein at 48 h increased significantly in icaritin-treated group, compared with that in control group (P<0.05).Icaritin can inhibit proliferation and induce apoptosis of THP-1 in vitro, Icaritin may induce apoptosis in THP-1 cells through the mitochondrial pathway.
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