ABSTRACT
Objective: To study the effects of ganoderma lucidum A on the proliferation and apoptosis of human inflammatory breast cancer SUM149 cells in vitro, and to clarify their mechanisms. Methods: The human inflammatory breast cancer SUM149 cells were divided into control group and different concentrations (0. 1, 0. 5, 1.0, 5. 0 and 10. 0 μmol · L-1) of ganoderma lucidum A groups; four holes were set up, and the samples were taken at 24, 48 and 72 h after culture. MTT assay was used to detect the inhibitory rate of proliferation of SUM149 cells. Flow cytometry was used to detect the apoptotic rate and cell cycle of SUM149 cells. The expression levels of Ki67 and Livin proteins in SUM149 cells were detected by immunocytochemical staining. Results: Compared with 0. 1 μmol · L-1 ganoderma lucidum A group, the inhibitory rates of proliferation of SUM149 cells in other concentrations of ganoderma lucidum A groups were significantly increased detectde by MTT method (P<0. 05 or P<0. 01) in a concentration- and time-dependent manner. The flow cytometry results showed that the apoptotic rates of SUM149 cells in different conventrations of ganoderma lucidum A groups were significantly higher than that in control group (P<0. 05 or P<0. 01) in a concentration- and time-dependent manner; at the same time, the cell cycle changed significantly. With the increase of ganoderma lucidum A of the concentration of ganoderma lucidum A, the pencentages of cells at G1 phase in different concentrations of ganoderma lucidum A groups were increased (P<0. 05), and the percentages of cells at S phase were decreased compared with control group (P<0. 05 or P<0. 01). The expression levels of Ki67 and Livin proteins in different concentrations of ganoderma lucidum A groups were decreased compared with control group (P<0. 05). Conclusion: Ganoderma lucidum A can inhibit the proliferation of human inflammatory breast cancer SUM149 cells through induction of apoptosis.
ABSTRACT
Objective:To study the effects of ganoderma lucidum A on the proliferation and apoptosis of human inflammatory breast cancer SUM149 cells in vitro,and to clarify their mechanisms.Methods:The human inflammatory breast cancer SUM149 cells were divided into control group and different concentrations (0.1,0.5,1.0,5.0 and 10.0 μmol · L-1) of ganoderma lucidum A groups;four holes were set up,and the samples were taken at 24,48 and 72 h after culture.MTT assay was used to detect the inhibitory rate of proliferation of SUM149 cells.Flow cytometry was used to detect the apoptotic rate and cell cycle of SUM149 cells.The expression levels of Ki67 and Livin proteins in SUM149 cells were detected by immunocytochemical staining.Results:Compared with 0.1 μmol · L-1 ganoderma lucidum A group,the inhibitory rates of proliferation of SUM149 cells in other concentrations of ganoderma lucidum A groups were significantly increased detectde by MTTmethod (P＜0.05 or P＜0.01) in a concentration-and time-dependent manner.The flow cytometry results showed that the apoptotic rates of SUM149 cells in different conventrations of ganoderma lucidum A groups were significantly higher than that in control group (P＜ 0.05 or P＜ 0.01) in a concentration-and time-dependent manner;at the same time,the cell cycle changed significantly.With the increase of ganoderma lucidum A of the concentration of ganoderma lucidum A,the pencentages of cells at G1 phase in different concentrations of ganoderma lucidum A groups were increased (P＜0.05),and the percentages of cells at S phase were decreased compared with control group (P＜0.05 or P＜0.01).The expression levels of Ki67 and Livin proteins in different concentrations of ganoderma lucidum A groups were decreased compared with control group (P＜0.05).Conclusion:Ganoderma lucidum A can inhibit the proliferation of human inflammatory breast cancer SUM149 cells through induction of apoptosis.
ABSTRACT
Malignant transformation of ovarian endometriosis is known as endometriosis associated ovarian cancer (EAOC). However, the carcinogenic pathways by which EAOC develops remained poorly understood, and numerous studies found the risk factors of malignant transformation. Recent studies have provided evidence that estrogen receptor-β(ER-β) can influence the proliferation, motility and apoptosis of ovarian cancer cells. The signal pathway of tyrosine kinase receptor-B (TrkB)/brain-derived neurotrophic factor (BDNF) has a direct relation with the endometriosis, and its anti-anoikis plays a prerequisite role in proliferation of cancer. In the nervous system, estradiol and estrogen receptor can be combined through a variety of ways to promote BDNF/TrkB high expression and activity enhancement. Therefore,the relationship between high-risk factors of malignant transformation and ER-β expression and ER-β and TrkB/BDNF signal pathways need to be explored in EAOC.