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Objective: To explore the apoptotic effect of baicalein, a coumarin flavonone, on human ovarian carcinoma HO-8910 cells, as well as the mechanisms. Methods: HO-8910 cells were treated with esculetin at a series of concentrations for different times. Expression of apoptosis related Bax/Bcl-2, and Caspases proteins in esculetin treated HO-8910 cells were detected by Western blotting. Cell growth and apoptosis were measured by MTT test and flow cytometry in vitro. Results: Cell viability assay showed that esculetin had obvious anti-proliferation effects on HO-8910 cells in a dose- and time-dependent manner. Compared with control group, the group treated with esculetin showed a significant increase in apoptosis rate (P < 0.05, P < 0.01). The results demonstrated that esculetin up-regulated the Bax/Bcl-2 ratio and cleaved Caspase-3, cleaved Caspase-9 expression in a dose-dependent manner. Conclusion: In summary, baicalein exerts anti-growth and induced-apoptosis activity against ovarian cancer HO-8910 cells through activating Caspase and Bcl-2 family proteins, therefore presenting as a promising therapeutic agent for the treatment of ovarian cancer.
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Ovarian cancer is one of the most common causes of death from gynecologic tumors and is an important public health issue. Ghrelin is a recently discovered bioactive peptide that acts as a natural endogenous ligand of the growth hormone secretagogue receptor (GHSR). Several studies have identified the protective effects of ghrelin on the mammalian reproductive system. However, little research has been done on the effects of ghrelin on ovarian cancer cells, and the underlying mechanisms of these effects. We sought to understand the potential involvement of mitogen-activated protein kinases (MAPKs) in ghrelin-mediated inhibition of growth of the ovarian line HO-8910. We applied different concentrations of ghrelin and an inhibitor of the ghrelin receptor (D-Lys3-GHRP-6) to HO-8910 cells and observed the growth rate of cells and changes in phosphorylation of the MAPKs ERK1/2, JNK and p38. We discovered that ghrelin-induced apoptosis of HO-8910 cells was though phosphorylated ERK1/2, and that this phosphorylation (as well as p90rsk phosphorylation) was mediated by the GHSR. The ERK1/2 pathway is known to play an essential part in the ghrelin-mediated apoptosis of HO-8910 cells. Hence, our study suggests that ghrelin inhibits the growth of HO-8910 cells primarily through the GHSR/ERK pathway.
Asunto(s)
Humanos , Femenino , Persona de Mediana Edad , Regulación Neoplásica de la Expresión Génica/genética , Ghrelina/farmacología , Sistema de Señalización de MAP Quinasas/fisiología , Neoplasias Ováricas/genética , Apoptosis/efectos de los fármacos , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Oligopéptidos/metabolismo , Neoplasias Ováricas/metabolismo , Fosforilación/efectos de los fármacos , Receptores de Ghrelina/antagonistas & inhibidores , Receptores de Ghrelina/metabolismo , Células Tumorales CultivadasRESUMEN
Objective To establish a human ovarian cancer cell line stably expressing enhanced green fluorescent protein(EGFP), so as to carry out visualized research on whole ovarian cancer. Methods We transfected human ovarian cancer cell line HO8910PM by gene transfection, and obtained cells stably expressing EGFP by sub-cloning amplification and selection with G418-resistance.The expression rate of EGFP was analyzed by flow cytometry (FC).The growth curve, adhesion, migration and invasion experiments were employed to study the biological behaviors of the cells transfected with EGFP. Results Flow cytometry results showed that EGFP positive rate of screened EGFP-HO8910PM cells was higher than 99%. The cell growth, adhesion, invasion and migration abilities of cells were not significantly changed after transfection. Conclusion We have successfully established a cell line EGFP-HO8910PM stably expressing EGFP and at mean time maintaining the characteristics of the parent cell line, which lays a foundation for whole-body visualization research of human ovarian cancer in vivo.
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Objective In many types of epithelial tumors,down-regulation or mutation of the epithelial cell-adherent molecule E-cadherin is associated with an increased invasiveness that can be prevented by the forced expression of the cell-adherent molecule.This suggests that E-cadherin is a latestage tumor suppressor that prevents invasion and metastasis.This study was to investigate cell invasion and migration status of human ovary serous cystadeno carcinoma HO-8910 cell line when the E-cadherin expression was down-regulated with RNA interference(RNAi) technology. Methods E-cadherin siRNA was transfected into HO-8910 cells to inhibit the expression of E-cadherin.The effect of RNAi was detected by immunofluoresence assay and Western blotting.The invasive ability of the cancer cells was determined by Transwell assay. Results After RNAi,the expressions of E-cadherin were significantly decreased from 63.7% to 11.9%(P