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BACKGROUND: The preventive and therapeutic medical utilization of this plant is an age-long practice across the globe. This study aimed to validate the impact of dark purple blossoms of basil (Ocimum basilicum L.) aqueous extract at low temperature (0 °C) mediated mitochondrial fission contributed to induced apoptosis in human breast cancer cells. METHODS: Fresh blossoms were extracted at low temperature (0 °C) using a watery solvent. Human MCF7 breast cancer cells were then treated with 3 separate fluctuated concentrations of 0, 50, 150 and 250 µg/mL for 24 and 48 h. RESULTS: The outcomes demonstrated the presence of anthocyanins, anthraquinones, tannins, reducing sugars, glycosides, proteins, amino acids, flavonoids and volatile oils and nonappearance of Terpinoids and alkaloids. Contrastingly, frail presence of steroids in basil blossoms aqueous concentrate was noted. In addition, the results from a phytochemical subjective examination of basil (Ocimum basilicum L.) blossoms aqueous extract demonstrated that most of the credited natural impacts containing more remarkable contents of antioxidants and anticancer compounds in basil blossoms aqueous extract. Moreover, the restraint of glucose take-up was alleviated mediated by a dose-dependent manner in MCF7 cells with basil (Ocimum basilicum L.) blossoms aqueous extract inducted for 24 h, resulting in mitochondrial fission. CONCLUSION: This is the first study that shows the impact of the aqueous extract of basil (Ocimum basilicum L.) blossoms was extracted at low temperature (0°C/6 h) underlined high amounts of flavonoids and phenolic compounds bearing more anticancer and antioxidant activities compared to another aqueous extract (using boiled water solvent) and alcoholic extracts.
Subject(s)
Humans , Plant Extracts/pharmacology , Apoptosis , Ocimum basilicum/chemistry , Flowers/chemistry , Mitochondrial Dynamics , Breast Neoplasms , Cold Temperature , MCF-7 CellsABSTRACT
A popular approach for the study of estrogen receptor α inhibition is to investigate the protein-protein interaction between the estrogen receptor (ER) and the coactivator surface. In our study, we investigated phytochemicals from Rubus coreanus that were able to disrupt ERα and coactivator interaction with an ERα antagonist. The E-screen assay and molecular docking analysis were performed to evaluate the effects of the estrogenic activity of R. coreanus extract and its constituents on the MCF-7 human breast cancer cell line. At 100 µg/mL, R. coreanus extract significantly stimulated cell proliferation (574.57 ± 8.56%). Sanguiin H6, which was isolated from R. coreanus, demonstrated the strongest affinity for the ERα coactivator-binding site in molecular docking analysis, with a binding energy of
Subject(s)
Humans , Breast Neoplasms , Cell Line , Cell Proliferation , Estrogens , Molecular Docking Simulation , Phytochemicals , RubusABSTRACT
Objective:To screen fatty acid synthase (FAS) inhibitors from natural products and study their inhibitory effects on the proliferation of MCF-7 breast cancer cells.Methods: CCK-8 method was used to detect the inhibitory effects of Fructus Amomi, Polygonum cuspidatum Sieb, Cinnamomi Ramulus and their main compounds, such as polydatin, resveratrol and cinnamic acid on the proliferation of MCF-7 breast cancer cells for 24 h.Results: The results showed that the IC50 values of the 60% ethanol extracts of Fructus Amomi, Polygonum cuspidatum Sieb, and Cinnamomi Ramulus were 24.86μg/ml, 153.67 μg/ml and 178 μg/ml respectively. The IC50 value of Resveratrol was 61.75 μg/ml. The inhibitory effect of Resveratrol was better than that of Polygonum cuspidatum Sieb. Cinnamic acid, the main component of Cinnamomi Ramulus had better inhibitory activity at lower concentration.Conclusion: The 60% ethanol extracts of Fructus Amomi, Polygonum cuspidatum Sieb, and Cinnamomi Ramulus all showed inhibitory effects on the proliferation of MCF-7 breast cancer cells in a dose-dependent manner. Among them, Fructus Amomi had the best inhibitory activity.
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6-Gingerol exerts anti-tumor effects in various cancer cell models. We evaluated the effect of 6-gingerol on the growth of MCF-7 breast cancer cells and MCF-10A breast epithelial cells to determine whether any growth-inhibitory effects found were attributable to apoptosis, and to elucidate the underlying mechanism of action. 6-Gingerol inhibited the viability of both cell lines in a dose- and time-dependent manner; however, the degree of inhibition was greater in MCF-7 than MCF-10A cells. By flow cytometry, induction of dose- and time-dependent apoptosis was found, and the magnitude of apoptosis was also markedly greater in MCF-7 than MCF-10A cells. Expression of caspase-3 and poly (ADP-ribose) polymerase (PARP) was observed in MCF-7 cells treated with 6-gingerol, and further cleavage of PARP occurred in these cells. We suggest that 6-gingerol induces apoptosis in human breast cancer cells mainly by promoting caspase-3 expression and subsequent degradation of PARP.
Subject(s)
Humans , Apoptosis , Breast Neoplasms , Breast , Caspase 3 , Cell Line , Epithelial Cells , Flow Cytometry , MCF-7 CellsABSTRACT
Objective:To study the expression and significance of Y14 and Upf1 in human breast cancer cells and breast epithelial cell. Methods:Western blotting and RT-PCR were applied to detect the expression of Y14 and Upf1 in human breast cancer cells(MCF-7,ZR-75-30,T47D,MDA-MB-435s,MDA-MB-453,MDA-MB-231)and breast epithelial cell(HBL-100). Results:Y14 and Upf1 levels of the breast cancer cells were obviously higher than that of breast cell(P
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Objective: This study was to explore the effects of phosphatase activity of PTEN (phosphatase and tensin homolog deleted on chromosome 10) on migration ability of human breast cancer ZR-75-1 cells. Methods: Three kinds of plasmids, wt-PTEN plasmid, G129R-PTEN plasmid, and G129E-PTEN plasmid, were constructed and transfected into human breast cancer cell line ZR-75-1, with a deletion of PTEN gene, via liposome mediation. The expression of PTEN protein as well as the Tyr397 in phospho-focal adhesion kinase (p397.FAK) was measured by Western blotting. The effect of phosphatase activity of PTEN was observed in a cell scratch wound model in vitro. The inhibitory effects of phosphatase activity of PTEN were measured by using cell-matrix adhesion test and reconstituted basement membrane invasion technique. The expression level of MMP-2 was determined by immunohistochemical staining. Results: Three kinds of plasmids (wt-PTEN, G129R-PTEN, and G129E-PTEN) were successfully transfected into ZR-75-1 cells, respectively. All the three stably transfected cells had PTEN protein expression. Transfection of wt-PTEN and G129R-PTEN inhibited the migration of ZR-75-1 cells. There was significant difference in the inhibitory degree of cell adhesion and invasion between wt-PTEN or G129E-PTEN groups and G129R-PTEN transfected or non transfected groups (P < 0.01). The level of p397.FAK was significantly lower in wt-PTEN and G129E-PTEN groups compared with G129R-PTEN transfected groups. There was significant difference in the expression level of MMP-2 between G129R-PTEN-transfected and non transfected groups(P < 0.01). Conclusion: Both wild-type PTEN with dual specific phosphatase activities and G129E-PTEN with only protein phosphatase activity have inhibitory effects on migration of human breast cancer cell line ZR-75-1. However G129R-PTEN without phosphatase activity have no effects.
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Aim To investigate the effect of exposure to high or low concentration chemotherapeutic drugs on multidrug resistance of human breast cancer cell MDA-MB-231.Method MDA-MB-231 was treated with high dose of adriamycin and paclitaxel or with low concentration of paclitaxe.SRB assay was used to determine the IC50 and RF.HE assay was used to evaluate the cellular morphology.The variations of P-gp and MDR1 were analyzed by immunocytochemistry and RT-PCR respectively.Results Cells survived only after treated with high dose of paclitaxel (MDA-MB-231/a).SRB assay showed that the growth rate of MDA-MB-231/a was the same as that of parent MDA-MB-231/w.The IC50 of the cells(MDA-MB-231/b)treated with low concentration of paclitaxel to several chemotherapeutic drugs was a little higher than that of MDA-MB-231/w.Immunocytochemistry showed that there was no difference between MDA-MB-231/a and MDA-MB-231/w in the expression of P-gp while the P-gp expression was a little higher in MDA-MB-231/b.RT-PCR assay showed that the MDR1 gene was over-expressed in MDA-MB-231/b.Conclusions The multidrug resistance cell lines can not be derived from MDA-MB-231/w by high dose of chemotherapeutic drugs.Induction of multidrug resistance response to chemotherapeutic drugs is related with transient exposure to low concentration of paclitaxel and this may be a way to establish the multidrug resistance model of MDA-MB-231 cells.
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Purpose:To study the RNA interference-mediated inhibition of survivin gene on the proliferation of human breast cancer SKBr-3 cells. Methods:SKBr-3 cells were transfected with a pSUPER-S1 vector plasmid that expressed survivin-targeted small interfering RNA, and the mRNA and protein levels of survivin gene were measured with RT-PCR and indirect immunofluorescence, respectively. The proliferation of transfected SKBr-3 cells was investigated through colony forming assay and MTT assay. The cell cycle phases were determined by flow cytometry(FCM). Results:The mRNA and protein levels of survivin declined markedly in pSUPER-S1-transfected SKBr-3 cells. And the colony forming rate of those cells(38?16.70)% was significantly lower than that of the control cells(90.3?4.04)%.The growth of the pSUPER-S1-transfected cells was decelerated and the cell cycle was mainly blocked at G_(1) phase(74.03?8.91)%. Conclusions:survivin gene silencing by RNA interference contributed to a distinctive inhibition of the proliferation of human breast cancer SKBr-3 cells in vitro.