ZFP36L2, a novel AML1 target gene, induces AML cells apoptosis and inhibits cell proliferation
Jia LiuWenting LuShuang LiuYing WangSaisai LiYingxi XuHaiyan XingKejing TangTian ZhengQing RaoMin WangJianxiang Wang
18
Citation
25
Reference
10
Related Paper
Citation Trend
Keywords:
Phenylbutyrate
Histone deacetylase inhibitor
Suberoylanilide hydroxamic acid (SAHA), a potent pan-histone deacetylase (HDAC) inhibitor, has been clinically approved for the treatment of cutaneous T-cell lymphoma (CTCL). SAHA has also been shown to exert a variety of anticancer activities in many other types of tumors, however, few studies have been reported in large-cell lung carcinoma (LCC). Our study aimed to investigate the potential antitumor effects of SAHA on LCC cells. Here, we report that SAHA was able to inhibit the proliferation of the LCC cell line NCI-H460 in a dose- and time-dependent manner, induced cell apoptosis and G2/M cell cycle arrest, decreased AKT and ERK phosphorylation, inhibited the expression of pro-angiogenic factors (VEGF, HIF-1α) in vitro, and suppressed tumor progression in an NCI-H460 cell nude mouse xenograft model in vivo. These results indicate that SAHA can exert its strong antitumor effects in LCC patient.
Histone deacetylase inhibitor
Vorinostat
Cite
Citations (26)
Objective To investigate the proliferation inhibition and apoptosis of human liver cancer Bel-7402cell line induced by GA in vetro.Methods The cell proliferation was determined by MTT assay.The cell apoptosis and cell cycle were analyzed by flow cytometry.The expressions of Bcl-2and Bax mRNA and protein were detected by RT-PCR and Western blot,respectively.Results GA inhibited the proliferation of Bel-7402cells in the does-and time-dependent manners.As the concentration of GA increased,the apoptosis rate of the cells increased.Meanwhile,GA induced G2 /M cell cycle arrest.The expressions of Bax mRNA and protein were upregulated while those of Bcl-2 were downregulated.Conclusion GA inhibits cell proliferation and enhances cell apoptosis,which may be related to the upregulation of Bax gene expression,downregulation of Bcl-2gene expression and the cell cycle arrest.
Gambogic acid
Cite
Citations (0)
Histone deacetylase inhibitor
Vorinostat
Epidermoid carcinoma
Growth inhibition
Cite
Citations (17)
Abstract In this review, we consider apoptosis as a process intimately linked to the cell cycle. There are several reasons for thinking of apoptosis as a cell cycle phenomenon. First, within the organism, apoptosis is almost exclusively found in proliferating tissues. Second, artificial manipulation of the cell cycle can either prevent or potentiate apoptosis, depending on the point of arrest. Data from such studies have suggested that molecules acting late in G1 are required for apoptosis. Since passage through late G1 into S phase in mammalian cells is known to be regulated by p53 and by activation of cyclin‐dependent kinases, we also examine recent studies linking these molecules to the apoptotic pathway.
Cite
Citations (432)
Objective To explore the effect of Tanshinone ⅡA on cell proliferation,apoptosis and cell cycle of fibroblasts derived from keloid.Methods Fibroblasts derived from keloid were cultured with different concentration of Tanshinone ⅡA(0 μg/mL,50 μg/mL,100 μg/mL and 200 μg/mL) in vitro.CCK-8 was used to detect cell proliferation,and flow cytometry was used to analyze cell apoptosis,cell cycle at the different time.Results Cell proliferation of fibroblasts derived from keloid was decreased,apoptosis at the early phase was increased,and cell cycle in G0/G1 phase was arrested by different concentration of Tanshinone ⅡA with different intervention time(P0.001),especially in 200 μg/mL group.Variance analysis showed that those differences have statistical significance.Conclusion Tanshinon ⅡA can suppress cell proliferation,induce cell apoptosis and arrest cell cycle of fibroblasts derived from keloid.The effect of Tanshinone ⅡA was affected by different concentration and different intervention time.
Keloid
Cell counting
Cite
Citations (0)
Objective To investigate the effects of a novel ruthenium(Ⅱ) polypyridyl complex △-[Ru (phen)2MCMIP]2 + (△-1) on proliferation and apoptosis of human osteosarcoma cell line MG-63 in vitro.Methods Cell counting of kit-8 (CCK-8) assay was used to detect the proliferation of MG-63 cells after 24,48,72h treatment with △-1 under the concentrations of 0.00,12.50,25.00,50.00,100.00,150.00 μmol/L;Changes of apoptosis and cell cycle in MG-63 cells after 24 h treatment of 0.00,25.00,50.00,100.00 μmol/L A-1 were determined and analyzed by flow cytometry (FCM).Results Ruthenium (Ⅱ) polypyridyl complex A-1 could significantly inhibit the growth of MG-63 in a dose and time dependent manner; the IC50 of 24 h,48 h,72 h was 57.80μmol/L,45.27μmol/L,32.51μmol/L respectively; flow cytometry detection showed that A-1 induced 37.10％ of apoptosis,while only 1.06％ in control group,and arrested cell cycle at G0/G1 phase.Conclusion Ruthenium(Ⅱ) polypyridyl complex A-1 is able to inhibit proliferation and induce apoptosis in MG-63 cells and arrest cell cycle at G0/G1 phase.
Key words:
Ruthenium(Ⅱ) complex; MG-63 cells; Proliferation; Apoptosis; Cell cycle
Cell counting
Cytometry
Cite
Citations (0)
Objective::To investigate the effect of Berberine on the proliferation and apoptosis in two gastric cancer cell lines and one gastric epithelial cell line GES,and to elucidate the underlying mechanism.Methods:MTT assay was adopted to detect the proliferation state of cells,and FCM was performed to found the alterations of cell cycle and apoptosis.Furthermore,we examined the expression of proteins which were associated with cell cycle and apoptosis by Western blotting.Results:The growth of gastric cancer cells were inhibited by Berberine(P0.05);Berberine induced a dose-dependent inhibition of cell growth in all three cell lines,and 50μg/ml of Berberine induced 81.3% growth inhibition in gastric cancer cells.As shown by flow cytometry,a low concentration of Berberine(10μg/ml) could cause G0/G1 cell cycle arrest and cell apoptosis(P0.05).The result of Western blot indicated that Berberine suppressed the protein expression of Bcl-2,and up-regulate the protein expression of Bax and p53 in gastric cancer cells in a time-and dose-dependent manner.Conclusion:Berberine inhibits the growth of gastric cancer cells by inducing cell cycle arrest and apoptosis.The underlying mechanism was partly due to the down-regulaion of Bcl-2 and the up-regulation of Bax and p53 in a time-and dose-dependent manner.
Growth inhibition
MTT assay
G1 phase
Cite
Citations (5)
Objective:To explore the effects of Ambrolic acid(AmbA) on proliferation and apoptosis of human gastric cancer SGC-7901 cell line.Methods:MTT assay was used to observe the anti-proliferation effect of AmbA on SGC-7901 cells with morphological changes observed under optical microscopy at the same time.The apoptosis rates and cell cycle status of SGC-7901 cells treated by AmbA were determined by flow cytometry(FCM).Results:AmbA inhibited the proliferation of SGC-7901 cells in a dose and time-dependent manner.FCM analysis showed that cells were arrested in S phase and induced apoptosis dose-dependently.Conclusion:AmbA has significant antitumor activity in vitro.The potential mechanism of anti-proliferation effect caused by AmbA may be cell-cycle arrest in S phase and cell apoptosis.
MTT assay
Cite
Citations (2)
OBJECTIVE:To study the effect and mechanism of histone deacetylase inhibitors sodium butyrate (NaB) and the humanized antibody Trastuzumab upon the proliferation,cell cycle and apoptosis of SKBR3 breast cancer cell line.METHODS:SKBR3 cells were treated with NaB,Trastuzumab and NaB plus Trastuzumab.Cell proliferation was determined by MTT assay,cell cycle and apoptosis were assayed by flow cytometry.The expression of p27Kip1 was detected by Western Blot.RESULTS:NaB treatment significantly inhibited the proliferation of SKBR3 cells,and induced cell cycle arrest at G0/G1 and apoptosis,furthermore,NaB upregulated the expression of p27Kip1 in SKBR3 cells (P0.05).However,Trastuzumab single-drug exhibit the proliferative inhibition and cell cycle arrest effect only at the concentration of 20 μg/mL(P0.05),but had little influence on apoptosis and p27Kip1 expression (P0.05),whereas,NaB plus Trastuzumab could enhance the anti-cancer effect of NaB and upregulate p27Kip1 expression in SKBR3 cells (P0.05).CONCLUSION:Trastuzumab and NaB can synergistically inhibit the proliferation of SKBR3 breast cancer cell line,induce cell cycle G0/G1 arrest and apoptosis,which may be associated with the evaluated expression of p27Kip1.
SKBR3
Histone deacetylase inhibitor
Sodium butyrate
Cite
Citations (0)
Coumarin has a variety of biological activities and widely exists in plants. Biscoumarin, derived from coumarin, their synthetic methods and bioactivities of biscoumarins is the hotspot of the current research. In this study, we evaluated for the first time the anticancer of a synthetic biscoumarin (3,3'-(4-chlorophenyl)methylene)bis(4-hydroxy-2H-chromen-2-one, C3) on lung cancer cells and explored the related mechanism. C3 was simply prepared by 4-hydroxycoumarin and 4-chlorobenzaldehyde under ethanol. The structure of C3 was elucidated by various spectroscopic analyses. The antiproliferation effect of C3 was evaluated by the cell counting kit-8 assay. Cell cycle and apoptosis analysis were detected by flow cytometry. The expression of correlated proteins was determined using Western blotting. The result showed that C3 displayed a strong cytostatic effect on Lewis lung cancer (LLC) cells. C3 inhibited the proliferation of LLC cells, and induced G2/M phase cell cycle arrest. In addition, C3 possessed a significant reduction on cell apoptosis by increasing of RIP1 expression. Our data showed that C3 suppresses lung cancer cell proliferation and induces cell apoptosis, which is possibly involved with the RIP1.
Cite
Citations (2)