Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential ...Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential target is cell division cycle 20(CDC20),which has been implicated in oncogenesis.This study investigated the effect of the CDC20 inhibitor Apcin on EC and elucidated the underlying mechanism involved.Methods The effects of Apcin on EC cell proliferation,apoptosis,and the cell cycle were evaluated using CCK8 assays and flow cytometry.RNA sequencing(RNA-seq)was subsequently conducted to explore the underlying molecular mechanism,and Western blotting and coimmunoprecipitation were subsequently performed to validate the results.Animal studies were performed to evaluate the antitumor effects in vivo.Bioinformatics analysis was also conducted to identify CDC20 as a potential therapeutic target in EC.Results Treatment with Apcin inhibited proliferation and induced apoptosis in EC cells,resulting in cell cycle arrest.Pathways associated with apoptosis and the cell cycle were activated following treatment with Apcin.Notably,Apcin treatment led to the upregulation of the cell cycle regulator p21,which was verified to interact with CDC20 and consequently decrease the expression of downstream cyclins in EC cells.In vivo experiments confirmed that Apcin treatment significantly impeded tumor growth.Higher CDC20 expression was observed in EC tissue than in nonmalignant tissue,and increased CDC20 expression in EC patients was associated with shorter overall survival and progress free interval.Conclusion CDC20 is a novel molecular target in EC,and Apcin could be developed as a candidate antitumor drug for EC treatment.展开更多
Summary：To investigate the effects of ATRA, acitretin and tazarotene on the growth and apoptosis of human tongue squamous cell carcinoma cell line Tca8113. The effect of retinoids on growth of Tca8113 cells in vitro ...Summary：To investigate the effects of ATRA, acitretin and tazarotene on the growth and apoptosis of human tongue squamous cell carcinoma cell line Tca8113. The effect of retinoids on growth of Tca8113 cells in vitro was examined by MTT assay and Trypan blue exclusion assay. Cell cycle analysis, early apoptosis analysis with double staining with Annexin V-FITC and PI, and active caspase-3 analysis with the staining of FITC-conjugated monoclonal rabbit anli-active caspase-3 antibody were made by flow cytometer. Streptavidin-biotin complex （SABC） immunocytochemical assays were employed for the detections of Bax/Bcl-2 proteins expressions. Our results showed that the retinoids inhibited growth of Tca8113 cells in a dose-and time-dependent manner with maximal inhibition 24 h after treatment of 10 5 mol/L. 10^-5 mol/L retinoids altered cell cycle distribution of Tca8113 cells, revealing an increase in G0/G1-phase population, a decrease in S-phase population and the inhibition of G1/S switching. 10^-5 mol/L retinoids significantly induced apoptosis of Tca8113 cells （all P〈0.05）, elevated the cells population with detectable active caspase-3 （P〈 0.05 for all）, increased the number of cells forming Bax and decreased the number of cells forming Bcl-2 significantly （all P〈0.05）. Acitretin played a most prominent role among the retinoids. It is concluded that the inhibition of cell cycle progress of Tca8113 cells by ATRA, acitretin and tazarotene is one of the possible mechanisms for proliferation arrest of TcaS113 cells elicited by the retinoids. The retinoids mediate apoptosis in TcaS113 cells that may be caspase-dependent through mitochondria pathway. High concentration retinoids inhibit growth of Tca8113 cells in vitro by interfering with proliferation and inducing apoptosis of cells. Acitretin may be an alternative medicine for the prevention and treatment of tongue squamous cell carcinoma.展开更多
Objective:To observe the effect of the artesunate(ART) on cellular proliferation in vitro,to search for the possible anti-tumor mechanism of ART on endometrial carcinoma at the molecular level and to provide the exper...Objective:To observe the effect of the artesunate(ART) on cellular proliferation in vitro,to search for the possible anti-tumor mechanism of ART on endometrial carcinoma at the molecular level and to provide the experimental and theoretical foundations for the clinical applications of ART.Methods:The cell proliferation was observed by microscope;MTT was used to examine the effects of ART on proliferation of HEC-1B cells,and flow cytometric analysis was used to detect cell cycle and apoptosis.The human endometrial carcinoma HEC-1B cells were conventionally cultured;ART was administered with a concentration of 40 μg/ml before the total RNA were extracted.mRNA expression of Survivin,Caspase-3,N-Cadherin,E-Cadherin,Fibronectin1 and Cox-2 were detected using RT-PCR.Results:ART reduced proliferation in human endometrial carcinoma cell line HEC-1B in a dose-and time-dependent effect.The cells of G0/G1 stage were significantly increased(P<0.05),but the cells of G2/M stages were significantly decreased(P<0.05),so it has shown that the cell cycle was probably blocked in G0/G1 stage.After intervention with ART at 20 and 80 μg/ml for 48 h,cellular apoptosis rate respectively was(36.42±0.77)% and(11.77±0.58)%,and the difference was statistically significant compared with the control([6.64±0.19]%,P<0.01).The expression of Cox-2 mRNA in the ART group was lower than those of control group,yet the expression of Caspase-3 and E-Cadherin mRNA in the ART group was higher than those of control group.Conclusion:ART can inhibit HEC-1B cell growth and proliferation in a dose-and time-dependent manner.Furthermore,ART can induce apoptosis in a dose-dependent manner.ART is able to downregulate Cox-2 mRNA expression and to upregulate E-Cadherin and Caspase-3 mRNA expression.So we can conclude that ART could induce the endometrial carcinoma HEC-1B cell apoptosis and inhibit tumor cell proliferation.展开更多
文摘Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential target is cell division cycle 20(CDC20),which has been implicated in oncogenesis.This study investigated the effect of the CDC20 inhibitor Apcin on EC and elucidated the underlying mechanism involved.Methods The effects of Apcin on EC cell proliferation,apoptosis,and the cell cycle were evaluated using CCK8 assays and flow cytometry.RNA sequencing(RNA-seq)was subsequently conducted to explore the underlying molecular mechanism,and Western blotting and coimmunoprecipitation were subsequently performed to validate the results.Animal studies were performed to evaluate the antitumor effects in vivo.Bioinformatics analysis was also conducted to identify CDC20 as a potential therapeutic target in EC.Results Treatment with Apcin inhibited proliferation and induced apoptosis in EC cells,resulting in cell cycle arrest.Pathways associated with apoptosis and the cell cycle were activated following treatment with Apcin.Notably,Apcin treatment led to the upregulation of the cell cycle regulator p21,which was verified to interact with CDC20 and consequently decrease the expression of downstream cyclins in EC cells.In vivo experiments confirmed that Apcin treatment significantly impeded tumor growth.Higher CDC20 expression was observed in EC tissue than in nonmalignant tissue,and increased CDC20 expression in EC patients was associated with shorter overall survival and progress free interval.Conclusion CDC20 is a novel molecular target in EC,and Apcin could be developed as a candidate antitumor drug for EC treatment.
文摘Summary：To investigate the effects of ATRA, acitretin and tazarotene on the growth and apoptosis of human tongue squamous cell carcinoma cell line Tca8113. The effect of retinoids on growth of Tca8113 cells in vitro was examined by MTT assay and Trypan blue exclusion assay. Cell cycle analysis, early apoptosis analysis with double staining with Annexin V-FITC and PI, and active caspase-3 analysis with the staining of FITC-conjugated monoclonal rabbit anli-active caspase-3 antibody were made by flow cytometer. Streptavidin-biotin complex （SABC） immunocytochemical assays were employed for the detections of Bax/Bcl-2 proteins expressions. Our results showed that the retinoids inhibited growth of Tca8113 cells in a dose-and time-dependent manner with maximal inhibition 24 h after treatment of 10 5 mol/L. 10^-5 mol/L retinoids altered cell cycle distribution of Tca8113 cells, revealing an increase in G0/G1-phase population, a decrease in S-phase population and the inhibition of G1/S switching. 10^-5 mol/L retinoids significantly induced apoptosis of Tca8113 cells （all P〈0.05）, elevated the cells population with detectable active caspase-3 （P〈 0.05 for all）, increased the number of cells forming Bax and decreased the number of cells forming Bcl-2 significantly （all P〈0.05）. Acitretin played a most prominent role among the retinoids. It is concluded that the inhibition of cell cycle progress of Tca8113 cells by ATRA, acitretin and tazarotene is one of the possible mechanisms for proliferation arrest of TcaS113 cells elicited by the retinoids. The retinoids mediate apoptosis in TcaS113 cells that may be caspase-dependent through mitochondria pathway. High concentration retinoids inhibit growth of Tca8113 cells in vitro by interfering with proliferation and inducing apoptosis of cells. Acitretin may be an alternative medicine for the prevention and treatment of tongue squamous cell carcinoma.
文摘Objective:To observe the effect of the artesunate(ART) on cellular proliferation in vitro,to search for the possible anti-tumor mechanism of ART on endometrial carcinoma at the molecular level and to provide the experimental and theoretical foundations for the clinical applications of ART.Methods:The cell proliferation was observed by microscope;MTT was used to examine the effects of ART on proliferation of HEC-1B cells,and flow cytometric analysis was used to detect cell cycle and apoptosis.The human endometrial carcinoma HEC-1B cells were conventionally cultured;ART was administered with a concentration of 40 μg/ml before the total RNA were extracted.mRNA expression of Survivin,Caspase-3,N-Cadherin,E-Cadherin,Fibronectin1 and Cox-2 were detected using RT-PCR.Results:ART reduced proliferation in human endometrial carcinoma cell line HEC-1B in a dose-and time-dependent effect.The cells of G0/G1 stage were significantly increased(P<0.05),but the cells of G2/M stages were significantly decreased(P<0.05),so it has shown that the cell cycle was probably blocked in G0/G1 stage.After intervention with ART at 20 and 80 μg/ml for 48 h,cellular apoptosis rate respectively was(36.42±0.77)% and(11.77±0.58)%,and the difference was statistically significant compared with the control([6.64±0.19]%,P<0.01).The expression of Cox-2 mRNA in the ART group was lower than those of control group,yet the expression of Caspase-3 and E-Cadherin mRNA in the ART group was higher than those of control group.Conclusion:ART can inhibit HEC-1B cell growth and proliferation in a dose-and time-dependent manner.Furthermore,ART can induce apoptosis in a dose-dependent manner.ART is able to downregulate Cox-2 mRNA expression and to upregulate E-Cadherin and Caspase-3 mRNA expression.So we can conclude that ART could induce the endometrial carcinoma HEC-1B cell apoptosis and inhibit tumor cell proliferation.
