Objective: To prove the molecular mechanisms of Mahkota Dewa(Phaleria macrocarpa) in suppressing proliferation of human retinoblastoma cells through suppression of cell cycle's gene-regulators expression.Methods: ...Objective: To prove the molecular mechanisms of Mahkota Dewa(Phaleria macrocarpa) in suppressing proliferation of human retinoblastoma cells through suppression of cell cycle's gene-regulators expression.Methods: In this study, the molecular mechanism of anti-tumor effect of fractioned extract of Phaleria macrocarpa(DLBS1425) in human retinoblastoma cells Y-79 was investigated by measuring the tumor cells viability, the assessment of population profiles of tumor cells in the cell cycle, and the mRNA concentration of p16, p21, p53, cyclin D,cyclin E, and E2 F.Results: DLBS1425 showed an inhibition effects towards proliferation of Y-79 cell line.Inhibition of proliferation was shown by suppression of cell cycle progression.DLBS1425 downregulated cyclin E, a G1 phase regulator gene of cell cycle, in dosedependent manner without affecting p53–p21 pathway.In the other word, DLBS1425 inhibits cell proliferation through suppression of cyclin E independently towards conventional proliferation pathway.Conclusions: Our results suggest that DLBS1425 is a potential anticancer agent which targets genes involved in cell proliferation in human retinoblastoma cells which make it pharmacologically ideal for the prevention and/or treatment of retinoblastoma cancer.展开更多
The effects of the cyclin E expression levels on chemotherapeutic sensitivity of breast cancer cell line were explored. After the cyclin E expression was knockdown in MDA-MB-435 by RNA interference, FACS analysis and ...The effects of the cyclin E expression levels on chemotherapeutic sensitivity of breast cancer cell line were explored. After the cyclin E expression was knockdown in MDA-MB-435 by RNA interference, FACS analysis and SA-β-gal staining were used to evaluate the response sensitivity of breast cancer cells to DNA damage drugs （adriamycin, etc.）. Adriamycin could induce G1 arrest in cyclin E knockdown MDA-MB-435 breast cell line and increase the percentage of cell senescence in cyclin E knockdown MDA-MB-435 cells. It was suggested that cyclin E knockdown could increase the chemotherapeutic sensitivity of breast cancer cells to DNA damage drugs.展开更多
基金Supported by The Dexa Laboratories of Biomolecular Sciences(DLBS),PT.Dexa Medica,Cikarang,West Java,Indonesia,Grant No.135/MP/DLBS/2016
文摘Objective: To prove the molecular mechanisms of Mahkota Dewa(Phaleria macrocarpa) in suppressing proliferation of human retinoblastoma cells through suppression of cell cycle's gene-regulators expression.Methods: In this study, the molecular mechanism of anti-tumor effect of fractioned extract of Phaleria macrocarpa(DLBS1425) in human retinoblastoma cells Y-79 was investigated by measuring the tumor cells viability, the assessment of population profiles of tumor cells in the cell cycle, and the mRNA concentration of p16, p21, p53, cyclin D,cyclin E, and E2 F.Results: DLBS1425 showed an inhibition effects towards proliferation of Y-79 cell line.Inhibition of proliferation was shown by suppression of cell cycle progression.DLBS1425 downregulated cyclin E, a G1 phase regulator gene of cell cycle, in dosedependent manner without affecting p53–p21 pathway.In the other word, DLBS1425 inhibits cell proliferation through suppression of cyclin E independently towards conventional proliferation pathway.Conclusions: Our results suggest that DLBS1425 is a potential anticancer agent which targets genes involved in cell proliferation in human retinoblastoma cells which make it pharmacologically ideal for the prevention and/or treatment of retinoblastoma cancer.
基金This project was supported by a grant from National Natural Sciences Foundation of China (No. 30400432).
文摘The effects of the cyclin E expression levels on chemotherapeutic sensitivity of breast cancer cell line were explored. After the cyclin E expression was knockdown in MDA-MB-435 by RNA interference, FACS analysis and SA-β-gal staining were used to evaluate the response sensitivity of breast cancer cells to DNA damage drugs （adriamycin, etc.）. Adriamycin could induce G1 arrest in cyclin E knockdown MDA-MB-435 breast cell line and increase the percentage of cell senescence in cyclin E knockdown MDA-MB-435 cells. It was suggested that cyclin E knockdown could increase the chemotherapeutic sensitivity of breast cancer cells to DNA damage drugs.
