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
Two series of tanshinone ⅡA derivatives were synthesized and evaluated for their antitumor activities as Cdc25 phosphatase inhibitors. Most of them demonstrated potent Cdc25 inhibitory activity and powerful cytotoxic...Two series of tanshinone ⅡA derivatives were synthesized and evaluated for their antitumor activities as Cdc25 phosphatase inhibitors. Most of them demonstrated potent Cdc25 inhibitory activity and powerful cytotoxicity against A549 tumor cell line, producing IC50 values in very low micromolar range. At last, the preliminary SAR was discussed.展开更多
Our previous studies found that Zinc-finger protein 382(ZNF382)played as a tumor suppressor gene in esophageal and gastric cancers,and a positive correlation between the high expression of ZNF382 and better outcome in...Our previous studies found that Zinc-finger protein 382(ZNF382)played as a tumor suppressor gene in esophageal and gastric cancers,and a positive correlation between the high expression of ZNF382 and better outcome in breast cancer patients.However,the biological roles and mechanisms of ZNF382 in breast cancer remains unclear.We detected ZNF382 expression by reverse-transcription PCR(RT-PCR)and real-time quantitative PCR(qRT-PCR)in breast cancer cells and tissues,and explored the impacts and mechanisms of ectopic ZNF382 expression in breast cancer cells in vitro and in vivo,respectively.Our results revealed that ZNF382 was significantly down-regulated in breast cancer tissues compared with adjacent non-cancer tissues.Restoration of ZNF382 expression in silenced breast cancer cells not only inhibited tumor cell colony formation,viability,migration and invasion,and epithelial-mesenchymal-transition(EMT),but also induced apoptosis and G0/G1 arrest.In conclusion,ZNF382 could induce G0/G1 cell cycle arrest through inhibiting CDC25A signaling,and,inhibit cell migration,invasion and EMT by antagonizing ZEB1 signaling in breast cancer cells.展开更多
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.
基金support by program for New Century Excellent Talents in University (NCET)National Natural Science Foundation of China(No.305722321)Lab of Organic Functional Molecules,the Sino-French Institute of ECNU for supports.
文摘Two series of tanshinone ⅡA derivatives were synthesized and evaluated for their antitumor activities as Cdc25 phosphatase inhibitors. Most of them demonstrated potent Cdc25 inhibitory activity and powerful cytotoxicity against A549 tumor cell line, producing IC50 values in very low micromolar range. At last, the preliminary SAR was discussed.
基金supported by National Natural Science Foundation of China(No.81872380,81772869)Natural Science Foundation of Chongqing(No.2019ZX002,cstc2019jcjy-msxmX0861,cstc2020jcyj-bshX0025)+3 种基金Opening Foundation of Chongqing Key Laboratory of Molecular Oncology and Epigenetics(No.MOEL201702)Postdoctoral Science Fundation of China(No.2020M683262)National Key Research and Development Program of China(No.2017YFE0191700)HK RGC(No.GRF14115019).
文摘Our previous studies found that Zinc-finger protein 382(ZNF382)played as a tumor suppressor gene in esophageal and gastric cancers,and a positive correlation between the high expression of ZNF382 and better outcome in breast cancer patients.However,the biological roles and mechanisms of ZNF382 in breast cancer remains unclear.We detected ZNF382 expression by reverse-transcription PCR(RT-PCR)and real-time quantitative PCR(qRT-PCR)in breast cancer cells and tissues,and explored the impacts and mechanisms of ectopic ZNF382 expression in breast cancer cells in vitro and in vivo,respectively.Our results revealed that ZNF382 was significantly down-regulated in breast cancer tissues compared with adjacent non-cancer tissues.Restoration of ZNF382 expression in silenced breast cancer cells not only inhibited tumor cell colony formation,viability,migration and invasion,and epithelial-mesenchymal-transition(EMT),but also induced apoptosis and G0/G1 arrest.In conclusion,ZNF382 could induce G0/G1 cell cycle arrest through inhibiting CDC25A signaling,and,inhibit cell migration,invasion and EMT by antagonizing ZEB1 signaling in breast cancer cells.
