ABSTRACT
Colorectal cancer (CRC) is a disease with high incidence worldwide. As of 2018, it is the second leading cause of cancer deaths in the world. In Saudi Arabia, the incidence of this disease has been increasing in the younger population. Both genetic and lifestyle factors may have contributed to its increased incidence and pathogenesis. Monosodium glutamate (MSG) is a food flavor enhancer that can be found in many commercial foods, and it can sometimes be used as a substitute to table salt. MSG has been investigated for its possible genotoxicity, yielding controversial results. In the present study, the effect of MSG on cell viability and its effect on expression of APC, BECN1, and TP53 genes in SW620 and SW480 colon cancer cell lines were studied. TP53 is a tumor suppressor gene that functions in modifying DNA errors and/or inducing apoptosis of damaged cells, and both APC and BECN1 genes are involved in CRC and are of importance in cellular growth and metastasis. Cancer cell viability was analyzed using MTT assay, and the results showed a significant increase in the number of viable cells after 24h of treatment with MSG with different concentrations (0.5, 1.0, 10, 50, and 100mM). Moreover, gene expression results showed a significant increase in the expression levels of APC and BECN1 under specified conditions in both cell lines; conversely, TP53 showed a significant decrease in expression in SW620 cells. Thus, it can be concluded that MSG possibly confers a pro-proliferative effect on CRC cells.
O câncer colorretal (CCR) é uma doença com alta incidência mundial. Desde 2018, é a segunda principal causa de mortes por câncer no mundo. Na Arábia Saudita, a incidência dessa doença vem aumentando na população mais jovem. Tanto fatores genéticos quanto de estilo de vida podem ter contribuído para o aumento da sua incidência e patogênese. O glutamato monossódico (MSG) é um intensificador de sabor de alimentos que pode ser encontrado em muitos alimentos comerciais e às vezes pode ser usado como um substituto do sal de cozinha. O MSG tem sido investigado por sua possível genotoxicidade, produzindo resultados controversos. Neste estudo, foram estudados o efeito do MSG na viabilidade celular e seu efeito na expressão dos genes APC, BECN1 e TP53 em linhas de células de câncer de cólon SW620 e SW480. TP53 é um gene supressor de tumor que atua modificando erros de DNA e/ou induzindo apoptose de células danificadas, estando os genes APC e BECN1 envolvidos no CRC e sendo importantes no crescimento celular e metástase. A viabilidade das células cancerosas foi analisada por meio do ensaio MTT, e os resultados mostraram um aumento significativo no número de células viáveis após 24 h de tratamento com MSG em diferentes concentrações (0,5; 1,0; 10; 50 e 100mM). Além disso, os resultados da expressão gênica mostraram um aumento significativo nos níveis de expressão de APC e BECN1 sob condições especificadas em ambas as linhagens celulares. Por outro lado, TP53 mostrou uma diminuição significativa na expressão em células SW620. Assim, pode-se concluir que, possivelmente, o MSG confere um efeito pró-proliferativo às células CRC.
Subject(s)
Humans , Genes, APC , Sodium Glutamate/toxicity , Colorectal Neoplasms/geneticsABSTRACT
Abstract Colorectal cancer (CRC) is a disease with high incidence worldwide. As of 2018, it is the second leading cause of cancer deaths in the world. In Saudi Arabia, the incidence of this disease has been increasing in the younger population. Both genetic and lifestyle factors may have contributed to its increased incidence and pathogenesis. Monosodium glutamate (MSG) is a food flavor enhancer that can be found in many commercial foods, and it can sometimes be used as a substitute to table salt. MSG has been investigated for its possible genotoxicity, yielding controversial results. In the present study, the effect of MSG on cell viability and its effect on expression of APC, BECN1, and TP53 genes in SW620 and SW480 colon cancer cell lines were studied. TP53 is a tumor suppressor gene that functions in modifying DNA errors and/or inducing apoptosis of damaged cells, and both APC and BECN1 genes are involved in CRC and are of importance in cellular growth and metastasis. Cancer cell viability was analyzed using MTT assay, and the results showed a significant increase in the number of viable cells after 24 h of treatment with MSG with different concentrations (0.5, 1.0, 10, 50, and 100mM). Moreover, gene expression results showed a significant increase in the expression levels of APC and BECN1 under specified conditions in both cell lines; conversely, TP53 showed a significant decrease in expression in SW620 cells. Thus, it can be concluded that MSG possibly confers a pro-proliferative effect on CRC cells.
Resumo O câncer colorretal (CCR) é uma doença com alta incidência mundial. Desde 2018, é a segunda principal causa de mortes por câncer no mundo. Na Arábia Saudita, a incidência dessa doença vem aumentando na população mais jovem. Tanto fatores genéticos quanto de estilo de vida podem ter contribuído para o aumento da sua incidência e patogênese. O glutamato monossódico (MSG) é um intensificador de sabor de alimentos que pode ser encontrado em muitos alimentos comerciais e às vezes pode ser usado como um substituto do sal de cozinha. O MSG tem sido investigado por sua possível genotoxicidade, produzindo resultados controversos. Neste estudo, foram estudados o efeito do MSG na viabilidade celular e seu efeito na expressão dos genes APC, BECN1 e TP53 em linhas de células de câncer de cólon SW620 e SW480. TP53 é um gene supressor de tumor que atua modificando erros de DNA e/ou induzindo apoptose de células danificadas, estando os genes APC e BECN1 envolvidos no CRC e sendo importantes no crescimento celular e metástase. A viabilidade das células cancerosas foi analisada por meio do ensaio MTT, e os resultados mostraram um aumento significativo no número de células viáveis após 24 h de tratamento com MSG em diferentes concentrações (0,5; 1,0; 10; 50 e 100mM). Além disso, os resultados da expressão gênica mostraram um aumento significativo nos níveis de expressão de APC e BECN1 sob condições especificadas em ambas as linhagens celulares. Por outro lado, TP53 mostrou uma diminuição significativa na expressão em células SW620. Assim, pode-se concluir que, possivelmente, o MSG confere um efeito pró-proliferativo às células CRC.
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@#[Abstract] Objective: To investigate the expression of transgelin (TAGLN) in colorectal cancer (CRC) tissues and its effect on the proliferation, migration and invasion of CRC SW480 cells. Methods: Surgically resected CRC tissues and corresponding para-cancerous tissues of 97 CRC patients from May 2015 to August 2016 in the Affiliated Tumor Hospital of Zhengzhou University were collected; In addition, CRC cell lines SW620, SW480, HCT116 and normal colorectal mucosal cell line FHC were also collected for this study. Immunohistochemical staining was used to detect the expression of TAGLN in CRC tissues, and the correlation between TAGLN and patients’ clinicopathological features was analyzed. Quantitative Real-time quantitative polymerase chain reaction (qPCR) and Western blotting (WB) were used to detect the mRNA and protein expressions of TAGLN in CRC cell lines. si-TAGLN and si-Ctrl were respectively transfected into SW480 cells by liposome transfection method. The effects of silencing TAGLN on the proliferation, migration and invasion of SW480 cells were detected by CCK-8, Wound-healing assay and Transwell assay, respectively; and the expression of EMT-related proteins E-cadherin, N-cadherin and vimentin were detected by WB. Results: The positive expression rate of TAGLN in CRC tissues was significantly higher than that in para-cancerous tissues (P<0.01), and TAGLN expression was correlated with TNM stage, degree of tumor differentiation and lymph node metastasis in CRC patients (P<0.05 or P<0.01). The mRNA and protein expression levels of TAGLN in SW480 cells were significantly higher than those in FHC cells (all P<0.01). After TAGLN silence, the proliferation, invasion and migration ability of SW480 cells were significantly reduced (all P<0.01), the expression level of E-cadherin in SW480 cells was increased, while the expression levels of N-cadherin and vimentin were decreased (all P<0.01). Conclusion: TAGLN is highly expressed in CRC tissues and cells. Silencing TAGLN can inhibit the proliferation, invasion and migration of CRC cells, suggesting that TAGLN plays an important role in the occurrence and development of CRC.
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@#[Abstract] Objective: To investigate the effect and mechanism of sevoflurane on the proliferation and invasion of colon cancer SW480 cells and the growth of transplanted tumor in nude mice by regulating the phosphorylation of PI3K. Methods: Colon cancer SW480 cells were treated with sevoflurane and randomly divided into control group, 0.5% sevoflurane group, 1.0% sevoflurane group and 2.0% sevoflurane group for subsequent experiments. The proliferation ability of SW480 cells was detected by Clone formation assay, mRNA expression levels of MDM2 and survivin in cells were detected by RT-PCR, invasion ability of cells was detected by Transwell assay, and protein expression levels of MDM2, survivin, VEGF, PI3K, p-PI3K, AKT and p-AKT were detected by Western blotting. PI3K activator 740Y-P was added for verification. SW480 cell transplanted tumor model was constructed on nude mice, and the tumor mass was weighed. The positive expression rates of MDM2 and VEGF in the transplanted tumor tissues were detected by Immunohistochemistry. Results: As compared with the control group and the low-dose group, the clone formation rate of SW480 cells and the number of invaded cells in the 1.0% and 2.0% sevoflurane groups were significantly decreased (all P<0.01), the mRNA and protein levels of MDM2 in the cells were significantly increased (all P<0.01), while the mRNA and protein levels of survivin were significantly decreased (all P<0.01); and the protein levels of VEGF, p-PI3K/PI3K and p-AKT/AKT were significantly decreased (all P<0.01). 740Y-P could reverse the effect of sevoflurane on the proliferation, invasion and expression of proteins associated with the PI3K/AKT signaling pathway in SW480 cells. The mass of transplanted tumor in 2.0% sevoflurane group was significantly decreased (P<0.01), and the positive MDM2 expression rate in tumor tissues was significantly increased (P<0.01), while the positive VEGF expression rate was significantly decreased (P<0.01). Conclusion: Sevoflurane inhibits the proliferation and invasion of colon cancer SW480 cells and the growth of xenografts in nude mice possibly by inhibiting PI3K phosphorylation.
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Background: Colon cancer is a major cause of morbidity and mortality in the world. Juglone is a natural compound which has been isolated from Juglans mandshurica Maxim, and it has various pharmacological effects such as antiviral, antibacterial, and anticancer. In our study, we aimed to investigate the effect of juglone on CCL-228-SW 480 colon carcinoma cell line in monolayer and spheroid culture medium. Materials and Methods: The CCL-228-SW 480 cell lines were cultured in both monolayer and spheroid cultures. Cells were treated with juglone at 24, 48, and 72 h of incubation. ID50 inhibition was determined on the dose for juglone and after it was found 20 μM was applied to the cells to examine the effect of juglone on CCL-228-SW 480 colon carcinoma cell line. After Juglone was applied the BrdU marking index, Transferase dUTP Nick ends Labeling (TUNEL) assay, active caspase-3 assay, apoptosis-inducing factor (AIF) assay were determined by immunohistochemistry in both the monolayer and spheroid cultures. Results: The control group had a healthy pattern of S-phase fraction, and many of the CCL-228-SW 480 cells nuclei were observed to be positive for BrdU. Terminal Deoxynucleotidyl TUNEL-positive cells, active Caspase-3, and AIF were detected after treatment with juglone in both the monolayer and spheroid cultures. Conclusions: The dead cell count was higher in the CCL-228-SW 480 cell lines with juglone applied than in the controls. Juglone significantly inhibits the proliferation and induces the apoptosis of CCL-228-SW 480 cells in vitro
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@# Objective: To explore the effects of noscapine (Nos) on the expression of cadherin 17 (CDH17) in colon cancer SW480 cells and the mechanism of Nos on cell migration. Methods: SW480 cells were divided into the control group, empty vector (si-EV) group, CDH17 interference (si-CDH17) group, Nos treatment group, and CDH17 interference+Nos treatment (si-CDH17+Nos) group. Small interfering RNA (siRNA) was used to knockdown CDH17, and the selected concentration of Nos was (55.30±2.21) µg/ml (IC50). The mRNA expression of CDH17 was detected by qPCR; the apoptosis and migration abilities of SW480 cells were observed by Hoechst33258 staining and Transwell assay; the contents of VEGF, MMP2 and MMP9 in SW480 cells were measured by ELISA, and the protein expressions of CDH17, Wnt3a and β-catenin were determined by WB. Results: Compared with the control group, mRNA and protein expressions of CDH17 obviously decreased, cell apoptosis and migration significantly reduced, while the contents of VEGF, MMP2 and MMP9 as well as the protein expressions of Wnt3a and β-catenin significantly decreased in Nos treatment group, siCDH17 group and si-CDH17+Nos treatment group (all P<0.01).The effect of si-CDH17+Nos treatment was more significant than that of si-CDH17 (P<0.01). Conclusion: Nos induces apoptosis and inhibits the migration of human colon cancer SW480 cells, which may be related to the down-regulation of CDH17 expression and inhibition of the Wnt3a/β-catenin signaling pathway.
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@# Objective: To investigate the expression of long non-coding RNASNHG16 (lncRNASNHG16) in colorectal cancer (CRC) tissues and cells, and to explore the mechanism of its regulation on the expression of mitochondrial glycerol-3-phosphate acyltransferase (GPAM) via sponging miR-128-3p. Methods: Sixty pairs of colorectal cancerous tissues and para-cancerous tissues that resected from CRC patients, who underwent surgery in the Department of Anorectal Surgery, Gansu Provincial People’s Hospital during Jan. 2014 and Jan. 2017, were collected for this study; In addition, CRC cell lines (SW480, SW620, HCT116, Caco-2,DLD-1, HT29) and colonic epithelial cell line CCD841 were also collected for the study. The expression of SNHG16 in collected tissues and cell lines was determined by Real-time quantitative PCR (qPCR), and its correlation to the clinicopathological features of CRC patients was also analyzed. SW480 cells were transfected with miR-128-3p mimic, miR-128-3p inhibitor, and si-SNHG16, respectively, and then the mRNA expressions of miR-128-3p and SNHG16 were detected by qPCR, the protein expression of GPAM was determined by Western blotting, and the cell proliferation, apoptosis and invasion were detected by CCK-8 assay, colony formation assay, cell apoptosis assay and Transwell chamber assay, respectively. The binding between SNHG16 and miR-128-3p was validated with dual luciferase reporter gene assay and RNA Immunoprecipitation assay. For in vivo experiment, mouse model of SW480 cell exnograft was constructed, and the effect of SNHG16 knockdown on the growth of exnograft was observed. Results: SNHG16 was found to highly expressed in human CRC tissues and cell lines (all P<0.01), and SNHG16 expression level was associated with lymph node metastasis, Duke's stage and patients’survival (all P<0.01). Knockdown of SNHG16 significantly inhibited CRC cell proliferation and invasion, and induced apoptosis (all P<0.01); After SNHG16 knockdown, the volume of exnograft was obviously reduced (P<0.05). Dual luciferase reporter gene assay and RNA Immunoprecipitation assay validated the interaction between miR-128-3p and SNHG16, and they were negatively correlated with each other in CRC patients (P<0.01). The SNHG16 regulated the expression of its down-stream gene GPAM via endogenously sponging miR-128-3p. Conclusion: SNHG16 regulates GPAM expression in CRC cells by sponging miR-128-3p, and SNHG16 and miR-128-3p may serve as potential targets for the diagnosis and treatment of CRC.
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@# Objective: To investigate the effects and mechanisms of miR-126-5p on proliferation, migration, invasion and apoptosis of colon cancer SW480 cells. Methods: Cells were transferred with miR-126 mimic and pcDNA Notch2 (pc-Notch2) respectively or simultaneously. Real-time fluorescence quantitative PCR was performed to detect the expression of miR-126 and Notch2. The relationship of miR-126-5p and Notch2 was determined by luciferase reporter assay. The CCK-8 assay, wound healing assay, Transwell and flow cytometry were performed to examine cell proliferation, migration, invasion and apoptosis, respectively. The protein levels of Notch2, proliferating cell nuclear antigen (PCNA), cleaved Caspase-3, metalloproteinase-2 (MMP-2) and MMP-9 were measured by Western blotting. Results: miR-126 mimic significantly increased expression level of miR-126-5p but reduced the expression of Notch2 in SW480 cells (all P<0.01); in the meanwhile, a binding site with miR-126-5p was confirmed on Notch2. Up-regulating the expression of miR-126-5p inhibited cell proliferation and the expression of PCNA (P<0.01), increased the cell apoptosis rate and protein level of cleaved Caspase-3 notably (all P<0.01). Pc-Notch2 obviously alleviated the effects of miR-126 mimic on cell proliferation and apoptosis (all P<0.01). Furthermore, miR-126 mimic significantly decreased the wound healing rate and invasive cell numbers (all P<0.01), and down-regulated the expressions of MMP-2 and MMP-9 (P<0.01); pc-Notch2 alleviated the effects of miR-126 mimic on cell migration, invasion and the expressions of MMP-2 and MMP-9 (all P<0.01). Conclusion: miR-126-5p can attenuate proliferation, migration and invasive ability of colon SW480 cells via inhibiting the expression of Notch2.
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@# Objective: To explore the effect of shRNA interfering BAMBI (bone morphogenetic protein and activin membrane bound inhibitor) on the proliferation, apoptosis, invasion and migration of human colon cancer SW480 cells and the possible mechanisms. Methods: After successful transfection with sh-BAMBI in SW480 cells, the mRNA and protein epxressions of BAMBI were detected by qRT-PCR and Western blotting, respectively. Cell proliferation was measured by MTT; apoptosis was tested by Hoechst33258 staining; cell invasion was detected by transwell assay; and cell migration was measured by wound healing assay. The expressions of TGF-β/ Smad/2 signaling pathway related proteins were detected by Western blotting. Results: The mRNA and protein levels of BAMBI in shBAMBI group were lower than those of control group (P<0.05). Compared with control group, cell proliferation in sh-BAMBI group was obviously decreased (P<0.05), while apoptosis was obviously increased (P<0.01); in the meanwhile, cell invasion and migration in sh-BAMBI group were significantly reduced (P<0.05). In addition, the protein level of TGF-β and the ratio of p-Smad/2/ Smad/2 in shBAMBI group were significantly higher than those in control group (P<0.05). Conclusion: Interference of BAMBI by shRNA inhibits proliferation, invasion and migration but induces apoptosis of human colon cancer SW480 cells and activates TGF-β/Smad/2 pathway.
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Objective To study PPARγ inhibitor(GW9662) ,on colon cancer SW480 cell proliferation and apoptosis intervened by Nimesulide(N) in vitro ,in order to investigate the role of PPARγpathway in colon cancer cell proliferation inhibition and apop‐tosis promotion induced by Nimesulide .Methods Cells were divided into 4 groups ,namely :the control group ,GW9662 group (GW9662 0 .1 ,0 .5 ,1 .0 ,5 .0μmol/L) ,N group ,GW9662+N group .MTT assay and FCM were used to determine proliferation ,ap‐optosis and cell cycle of SW480 cells .And the expression of PPARγ,p21Waf1 ,p27Kip1 ,Bcl‐2 ,Bax ,VEGF proteins were measured by Western‐blot .Results N inhibited SW480 cells proliferation in a time‐dependent manner (P0 .05) . Cell apoptosis rate of group N increased significantly ,compared with control group(P<0 .01) .The apoptosis rates of SW480 cells incubated with Nimesulide and GW9662 dropped significantly compared with Nimesulide alone (P<0 .01) .Above results showed that GW9662 could attenuate the effect of nimesulide on cell apoptosis and cell cycle .The results of Western‐blot :Compared with the control group ,the expression of PPARγ,p21Waf1 ,p27Kip1 ,Bax protein were up‐regulated significantly in nimesulide group(P<0 .05 or P<0 .01) ,but Bcl‐2 and VEGF were down‐regulated significantly(P<0 .01) .Compared with the nimesulide group ,the expres‐sion of PPARγ,p21Waf1 , p27Kip1 and Bax protein were down‐regulated obviously in GW9662+N group(P<0 .05 or P<0 .01) .Corre‐spondingly ,Bcl‐2 and VEGF were up‐regulated obviously(P<0 .05) .Conclusion N could effectively inhibit SW480 cell prolifera‐tion and induce its apoptosis .PPARγpathway may play an important role in proliferation inhibition and apoptosis induced by Nime‐sulide in colon cancer cell .
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Background and purpose:As a new candidate tumor suppressor gene, p33ING1b has many biological functions. This study was done to investigate its role in the regulation of the proliferation of human colon cancer cell line SW480. Methods:The pcDNA3.1(+)/p33ING1b/SW480 cells were identified by Western blot and S-P immunohistochemical method. In order to elucidate the effect of expression of exogenous p33ING1b gene on the colorectal cancer cell SW480, the proliferation rates were analyzed by growth curves and colony formation assay in soft agar for cells including SW480, pcDNA3.1(+)/p33ING1b/SW480 and pcDNA3.1(+)/SW480. At same time, the apoptotic rate of cells and the cell cycle analysis were also tested by flow cytometry.Furthermore,using western blot analysis,we detected the expression level of the protein p53, p21WAF1,Bax and Bcl-2 in those three group cells, which initially indicate the molecule mechanism of inducing apoptosis by gene p33ING1b. Results:The cell growth rates of SW480 cells transfected with pcDNA3.1 (+)/p33ING1b were slower than those transfected with pcDNA3.1(+) or untransfected.The colony formation efficiency of pcDNA3.1(+)/p33ING1b/SW480 were decreased and the apoptotic rates were increased compared with pcDNA3.1(+)/SW480 and SW480(P0.05). Conclusion:After overexpression of exogenous p33ING1b protein in SW480 cell, there were inhibition of the proliferation rate and induction of apoptosis, the molecular mechanism might be associated with up- regulated expression of Bax and down-regulated expression of Bcl-2 by p33ING1b gene.
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Purpose:To investigate the effect of short hairpin RNA (shRNA) targeting CD44v3 on adhesion and invasion behavior of human colon cancer cell line SW480 induced by hyaluronan in vitro. Methods:RNA interference plasmid including U6 promoter and expressing shRNA of CD44v3 was designed, constructed, and transfected into SW480 cell line. CD44v3 expression was examined by reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Adhesive and invasive ability were examined by plate adhesion model and Boyden chamber model.Results:After plasmid transfection,CD44v3 expression in SW480 cell and the number of SW480 cell induced by hyaluronan adhesiving on plate or permeating septum of Boyden chamber decreased significantly (P
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Background and purpose:The most serious aspect of cancer is the emergence of metastases in organs distant from the primary tumor, since most deaths from cancer are due to metastases. In recent years, a series of studies has been undertaken both in vitro and in vivo, and demonstrated that the CD133+ hematopoietic stem cell is effective in increasing mice tumor cell metastases, but the efficacy of CD133+ stem cells is not well studied for human cancer.We investigated the effects of CD133+ stem cells on the proliferation, adhesion and migration in human colorectal neoplasm cell line SW480.Methods:CD133+ cells were separated from fresh cord blood mononuclear cells(MNC) by Ficoll density gradient centrifugation and magnetic activated cell-sorting system(MACS).The treatment group was the co-culture of CD133+ cells and SW480, the control group used the same culture medium without CD133+ cells. The effect of CD133+ cells on proliferation in SW480 cell was measured by MTT assay, the migration abilities of SW480 cell were assayed in Transwell cell culture, Cell adhesion assay was carried out in a 96 microplate well precoated with fibronection.Results:CD133+ cells could significantly improve the growth ability of SW480 cell, not only the ability of proliferation, but also the morphology. The morphology of the cells was remarkably changed. Irregular nucleus, double nucleus and polymorphic nucleus appeared in the treatment group, and the cells were shaped as polygon-like and leptosomatic. In the cell adhesion assay, A 490 of the treatment group was 0.11?0.01, A 490 of the control group was 0.05?0.01(P﹤0.05).Conclusions:Our results indicate that the CD133+ cell is effective in increasing tumor cell proliferation and invasion. Hematopoietic stem cell may play an important role in the invasion and metastasis of colorectal neoplasm.
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In this paper the procedure for the study of anticancer drug screenning on colon cancer cell line SW-480 using MTT (tetrazolium dye) assay has been observed in vitro. Our study showed that(l) The optimal target cell concentration was 1-5?10~4 cell/well. (2) The optimal MTT concentration is 5 mgml~(-1) when a range of 0-10 mgml~(-1) was tested. In view of the relatively small increase in sensitivity obtained after 6h, we chose 4h incubation as optiomal incubation time. (3) DMSO and acid isopropyl alcohol were both effective to dissolve the formazan produced but greater solubility and absorbance reading were seen using DMSO. (4) The addition of new born calf serum to the reaction mixture results in a gradual lowering of optical density than that produced by serum-free medium before the addition of DMSO.The assay is simple and rapid with a CV within groups about 10%. when using DMSO as a solvent in this assay, it is necessary to read the plates within 30 mim after adding DMSO. Meanwhile, the chemosensitivity of SW-480 cell to 72h exposrre to four kinds of standard anticancer drugs was different.
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Aim To investigate the arrest effect of diallyl disulfide(DADS) in the cell cycle of human nasopharyngeal carcinoma SW480 cell line and its molecular mechanism.Mothdes The growth inhibition effect of DADS of different concentrations on SW480 cell line was measured by MTT assay and cell counting.Phase distribution of cell cycle was analyzed by flow cytometry.Expression of Ubiquitin and FKBP was determined by Western blot.Results The MTT assay showed that DADS inhibited growth of SW480 cells significantly in a dose-dependent manner.Adding 25,35,50 and 70 mg?L-1 DADS for 48 hours,SW480 cell growth was suppressed by 18.67%,33.02%,49.12% and 66.86%,respectively.There were significant differences between the treated and controlled cases(P