CDC25A, TSSK3 and P53 expressions in vitro in cultured sertoli cells after FSH treatment were studied in order to provide some data for further researches of spermatogenesis. Different concentrations of FSH（0, 0.01, ...CDC25A, TSSK3 and P53 expressions in vitro in cultured sertoli cells after FSH treatment were studied in order to provide some data for further researches of spermatogenesis. Different concentrations of FSH（0, 0.01, 0.02, 0.04, and 0.08 IU ·m L^-1） were used to treat sertoli cells cultured in vitro. The expression of CDC25 A, TSSK3 and P53 was determined by real-time-PCR at 6 h,12 h and 24 h after FSH treatment of sertoli cells. The results showed that FSH had no significant effect on expression of CDC25A（p〈0.05）, could significantly improve the expression of TSSK3 and P53（p0.05）, and had no significant effect on expression of CDC25 A in sertoli cells, but it could significantly improve the expression of TSSK3. CDC25 A was likely to play a role in other signaling pathways in sertoli cells. Within the range of certain concentration of FSH, TSSK3 in sertoli cells had the highest expression at about 24 h. TSSK3 protein produced in sertoli cells was likely to play an important role in substrate-level phosphorylationbe in meiosis and mitosis of spermatogenic cells. FSH could promote P53 expression and the highest expression was at about 12 h, and P53 might control the division of spermatogenic cells as well as sertoli cells.展开更多
Objective:This study was to further investigate the effect of CDC25A gene on proliferation, invasion and metastasis of hepatocellular carcinoma HepG2 cells, and to explore whether CDC25A and IL6 interact in liver canc...Objective:This study was to further investigate the effect of CDC25A gene on proliferation, invasion and metastasis of hepatocellular carcinoma HepG2 cells, and to explore whether CDC25A and IL6 interact in liver cancer.Methods: HepG2 cells were transfected with lentiviral CDC25A-shRNA to specifically block the expression of CDC25A in the experimental group (KD group), transfected with lentiviral-negative shRNA as a negative control group (NC group), and the conventionally cultured HepG2 cells were blank control group (Control group). Real-time quantitative PCR and Western blot were used to detect the mRNA and protein expression levels of CDC25A and IL6.Results:The expression level of IL6 mRNA in the experimental group was 0.4650.026, which was significantly lower than that of the negative control group of 1.0940.179 and the blank control group of 1.0020.311. The difference was statistically significant(P<0.05). The protein expression level of IL6 was 0.4990.061, which was significantly lower than the negative control group of 1.3110.034 and the blank control group of 1.2530.035. The difference was statistically significant (P<0.05). Conclusions: The CDC25A gene in hepatoma HepG2 cells was silenced, while the expression of IL6 was down-regulated. CDC25A may play a role in the development and invasion of liver cancer by regulating the expression of IL6.展开更多
Objective To observe the effect of artesunate (Art) on the proliferation of human esophageal carcinoma cell line Eca109 and the growth of transplantation tumors of nude mice, and explore the possible involvement of CD...Objective To observe the effect of artesunate (Art) on the proliferation of human esophageal carcinoma cell line Eca109 and the growth of transplantation tumors of nude mice, and explore the possible involvement of CDC25A expression in the cell cycle arrest induced by Art. Methods MTT method was employed to detect the proliferation of the Eca109 cells and normal human peripheral blood mononuclear cells (hPBMC) after Art treatment. Cell cycle of the tumor cells was assayed by flow cytometry. Inhibitory effects of Art on the transplanted tumor on nude mice were observed by mass weight, volume and morphological method. The expression of CDC25A in the Eca109 cells was examined by RT-PCR and Western blotting. Results Art significantly inhibited the proliferation of Eca109 with the IC50 of (68.80±0.76) μmol/L, while it had weaker effect on that of the hPBMC induced by Con A. At lower doses of Art, the number of Eca109 cells during G0/G1 was increased, and that at S phase was reduced dramatically. However, when the concentration was up to 100 μmol/L, most of cells were arrested at G2/M phase. The volume and weight of transplanted tumor receiving Art treatment were smaller and lower than those of control group, with the maximal inhibitory rate of 76.4%. Art dramatically inhibited the mRNA as well as protein expressions of CDC25A in the Eca109 cells. Conclusion Art can inhibit the proliferation of tumor cells and transplanted tumor without apparent side effect, possibly by the mechanism of modulating cell cycle through CDC25A down-regulation.展开更多
基金Supported by the National International Scientific and Technological Cooperation Project(2011DFA30760-2-1)Fund of Key Laboratory of Northeast Agricultural University,China(GXZDSYS-2012-07)
文摘CDC25A, TSSK3 and P53 expressions in vitro in cultured sertoli cells after FSH treatment were studied in order to provide some data for further researches of spermatogenesis. Different concentrations of FSH（0, 0.01, 0.02, 0.04, and 0.08 IU ·m L^-1） were used to treat sertoli cells cultured in vitro. The expression of CDC25 A, TSSK3 and P53 was determined by real-time-PCR at 6 h,12 h and 24 h after FSH treatment of sertoli cells. The results showed that FSH had no significant effect on expression of CDC25A（p〈0.05）, could significantly improve the expression of TSSK3 and P53（p0.05）, and had no significant effect on expression of CDC25 A in sertoli cells, but it could significantly improve the expression of TSSK3. CDC25 A was likely to play a role in other signaling pathways in sertoli cells. Within the range of certain concentration of FSH, TSSK3 in sertoli cells had the highest expression at about 24 h. TSSK3 protein produced in sertoli cells was likely to play an important role in substrate-level phosphorylationbe in meiosis and mitosis of spermatogenic cells. FSH could promote P53 expression and the highest expression was at about 12 h, and P53 might control the division of spermatogenic cells as well as sertoli cells.
基金National Natural Science Foundation of China,Project No:81260080Guangxi Natural Science Foundation Project,Project No:2017GXNSFBA198003Basic Ability Improvement Project for Young and Middle-aged Teachers in Guangxi Zhuang Autonomous Region,Project No:2017KY0102.
文摘Objective:This study was to further investigate the effect of CDC25A gene on proliferation, invasion and metastasis of hepatocellular carcinoma HepG2 cells, and to explore whether CDC25A and IL6 interact in liver cancer.Methods: HepG2 cells were transfected with lentiviral CDC25A-shRNA to specifically block the expression of CDC25A in the experimental group (KD group), transfected with lentiviral-negative shRNA as a negative control group (NC group), and the conventionally cultured HepG2 cells were blank control group (Control group). Real-time quantitative PCR and Western blot were used to detect the mRNA and protein expression levels of CDC25A and IL6.Results:The expression level of IL6 mRNA in the experimental group was 0.4650.026, which was significantly lower than that of the negative control group of 1.0940.179 and the blank control group of 1.0020.311. The difference was statistically significant(P<0.05). The protein expression level of IL6 was 0.4990.061, which was significantly lower than the negative control group of 1.3110.034 and the blank control group of 1.2530.035. The difference was statistically significant (P<0.05). Conclusions: The CDC25A gene in hepatoma HepG2 cells was silenced, while the expression of IL6 was down-regulated. CDC25A may play a role in the development and invasion of liver cancer by regulating the expression of IL6.
文摘Objective To observe the effect of artesunate (Art) on the proliferation of human esophageal carcinoma cell line Eca109 and the growth of transplantation tumors of nude mice, and explore the possible involvement of CDC25A expression in the cell cycle arrest induced by Art. Methods MTT method was employed to detect the proliferation of the Eca109 cells and normal human peripheral blood mononuclear cells (hPBMC) after Art treatment. Cell cycle of the tumor cells was assayed by flow cytometry. Inhibitory effects of Art on the transplanted tumor on nude mice were observed by mass weight, volume and morphological method. The expression of CDC25A in the Eca109 cells was examined by RT-PCR and Western blotting. Results Art significantly inhibited the proliferation of Eca109 with the IC50 of (68.80±0.76) μmol/L, while it had weaker effect on that of the hPBMC induced by Con A. At lower doses of Art, the number of Eca109 cells during G0/G1 was increased, and that at S phase was reduced dramatically. However, when the concentration was up to 100 μmol/L, most of cells were arrested at G2/M phase. The volume and weight of transplanted tumor receiving Art treatment were smaller and lower than those of control group, with the maximal inhibitory rate of 76.4%. Art dramatically inhibited the mRNA as well as protein expressions of CDC25A in the Eca109 cells. Conclusion Art can inhibit the proliferation of tumor cells and transplanted tumor without apparent side effect, possibly by the mechanism of modulating cell cycle through CDC25A down-regulation.
