Introduction: Breast cancer is the most common cancer among women in the Philippines and about 3 in every 100 Filipina will be diagnosed with breast cancer in their lifetime. There is a need to discover safe, yet inexpensive herbal extracts with potential cytotoxic properties as potential treatment modalities to treat breast cancer. Objectives: This study seeks to explore the cytotoxic and apoptotic properties of the ethyl acetate fraction of the defatted crude methanol leaf extract of Syzygium samarangense in MCF-7 breast cancer cell lines. Methods: Screening for flavonoids of the extracts was performed using TLC, total flavonoids, total phenols, FTIR and LC-MS spectroscopy. The hydrogen peroxide and ferric reducing anti-oxidant power were used as substrates to assess in vitro anti-oxidative properties of the extracts. The MTT dye viability assay was used to assess the cytotoxic properties of the extracts against MCF-7 cells. Apoptotic properties of the extracts in MCF-7 cells were determined by caspase-3 activation assay, DNA fragmentation patterns and fluorescence microscopy after annexin-V and propidium iodide staining. Results: The abundance of flavonoids in the ethyl acetate fraction of the crude methanol leaf extract was established by TLC, FTIR, LC-MS/MS, total flavonoid and total phenol analyses. The in vitro anti-oxidative properties of this extract was comparable to ascorbic acid. The median inhibitory concentration (IC50) of this extract in MCF-7 breast cancer cell lines was 7.2 mcg/mL while doxorubicin registered an IC50 of 1.2 mcg/mL. At this concentration, the extract was not cytotoxic to normally-dividing breast epithelial cells. Cytotoxicity of the extract was mediated via apoptosis as demonstrated by DNA fragmentation, caspase-3 activation and fluorescence microscopic analyses. Conclusion The study shows that the flavonoid-rich ethyl acetate fraction of the crude methanol leaf extract of S. samarangense possesses potent apoptotic and cytotoxic properties against MCF-7 breast cancer cell lines at low concentrations.
MCF-7 Cells ; Syzygium

Introduction: Breast cancer is the most common cancer among women in the Philippines and about 3 in every 100 Filipina will be diagnosed with breast cancer in their lifetime. There is a need to discover safe, yet inexpensive herbal extracts with potential cytotoxic properties as potential treatment modalities to treat breast cancer. Objectives: This study seeks to explore the cytotoxic and apoptotic properties of the ethyl acetate fraction of the defatted crude methanol leaf extract of Syzygium samarangense in MCF-7 breast cancer cell lines. Methods: Screening for flavonoids of the extracts was performed using TLC, total flavonoids, total phenols, FTIR and LC-MS spectroscopy. The hydrogen peroxide and ferric reducing anti-oxidant power were used as substrates to assess in vitro anti-oxidative properties of the extracts. The MTT dye viability assay was used to assess the cytotoxic properties of the extracts against MCF-7 cells. Apoptotic properties of the extracts in MCF-7 cells were determined by caspase-3 activation assay, DNA fragmentation patterns and fluorescence microscopy after annexin-V and propidium iodide staining. Results: The abundance of flavonoids in the ethyl acetate fraction of the crude methanol leaf extract was established by TLC, FTIR, LC-MS/MS, total flavonoid and total phenol analyses. The in vitro anti-oxidative properties of this extract was comparable to ascorbic acid. The median inhibitory concentration (IC50) of this extract in MCF-7 breast cancer cell lines was 7.2 mcg/mL while doxorubicin registered an IC50 of 1.2 mcg/mL. At this concentration, the extract was not cytotoxic to normally-dividing breast epithelial cells. Cytotoxicity of the extract was mediated via apoptosis as demonstrated by DNA fragmentation, caspase-3 activation and fluorescence microscopic analyses. Conclusion The study shows that the flavonoid-rich ethyl acetate fraction of the crude methanol leaf extract of S. samarangense possesses potent apoptotic and cytotoxic properties against MCF-7 breast cancer cell lines at low concentrations.
MCF-7 Cells ; Syzygium

No abstract available.
Breast Neoplasms* ; Breast* ; Cell Proliferation* ; MCF-7 Cells ; Polyamines

From the pericarps of Litsea japonica (Thunb.) Jussieu, eighteen butanolide derivatives (1 – 18) were evaluated for their cytotoxic activity against HeLa, HL-60, and MCF-7 cells. Compounds 1 – 9 with 2-alkylidene-3-hydroxy-4-methylbutanolides structure exhibited cytotoxic activities against cancer-cell lines. Among them, compound 8 (litsenolide D₂) exhibited the most potent cytotoxicity against the tested cell lines, including HeLa, HL-60, and MCF-7, with IC₅₀ values of 17.6 ± 1.3, 4.2 ± 0.2, and 12.8 ± 0.0 µM, respectively. Compound 8 induced apoptosis in a dose-dependent manner. Annexin V/Propidium Iodide (PI) double staining confirmed that 8 effectively induced apoptosis in MCF-7 cells. To the best of our knowledge, we have reported cytotoxic activity of butanolides from L. japonica against these cancer-cell lines for the first time.
Apoptosis ; Cell Line ; Lactones ; Lauraceae ; Litsea ; MCF-7 Cells

Reserpine is a well-known medicine for the treatment of hypertension, however the role of reserpine in cell signaling is not fully understood. Here, we report that reserpine treatment induces the phosphorylation of AMP activated protein kinase (AMPK) at threonine 172 (T172) in PC12 cells. Phosphorylation of AMPK T172 is regulated by upstream signaling molecules, and the increase of phospho-T172 indicates that AMPK is activated. When we examined the FOXO3a dependent transcription by using the FHRE-Luc reporter assay, reserpine treatment repressed the FHRE-Luc reporter activity in a dose dependent manner. Finally, we showed that reserpine treatment induced the phosphorylation of AMPK as well as cell death in MCF-7 cells. These results suggest that AMPK is a potential cellular target of reserpine.
AMP-Activated Protein Kinases* ; Animals ; Cell Death ; Hypertension ; MCF-7 Cells ; PC12 Cells ; Phosphorylation ; Reserpine* ; Threonine

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.
Apoptosis ; Breast Neoplasms* ; Breast* ; Caspase 3 ; Cell Line ; Epithelial Cells ; Flow Cytometry ; Humans* ; MCF-7 Cells

In order to investigate in greater detail the two methods based on Hertz model for analyzing force-distance curve obtained by atomic force microscopy, we acquired the force-distance curves of Hela and MCF-7 cells by atomic force microscopy (AFM) indentation in this study. After the determination of contact point, Young's modulus in different indentation depth were calculated with two analysis methods of "two point" and "slope fitting". The results showed that the Young's modulus of Hela cell was higher than that of MCF-7 cell,which is in accordance with the F-actin distribution of the two types of cell. We found that the Young's modulus of the cells was decreased with increasing indentation depth and the curve trends by "slope fitting". This indicated that the "slope fitting" method could reduce the error caused by the miscalculation of contact point. The purpose of this study was to provide a guidance for researcher to choose an appropriate method for analyzing AFM indentation force-distance curve.
Actins ; Elastic Modulus ; HeLa Cells ; cytology ; Humans ; MCF-7 Cells ; cytology ; Microscopy, Atomic Force

The study investigated the chemical constituents from the whole herb of Carpesium cernuum. Three new diterpenoids were isolated from the whole herb of C. cernuum by column chromatography on silica gel, Sephadex LH-20, and semi-preparative HPLC. Their structures were identified by MS, NMR and other spectral techniques. The isolates were identified as(5Z)-2-oxo-2, 10, 14-trimethylhexadeca-5, 13-diene-11α, 18-diol(1),(2E, 10E)-7-[(acetyloxy)methyl]-3, 11, 15-trimethylhexadeca-2, 10, 14-triene-1, 12α-diol(2),(2E, 6Z)-3, 11, 15-trimethylhexadeca-2, 6, 14-triene-1, 12α, 19-triol(3), respectively. The cytotoxic activity of compounds 1-3 were investigated with DU-145, MCF-7, and A549 cells by MTT. The results showed that compound 1 and 3 had certain inhibitory effects on MCF-7 cells, with the inhibition rates of 45.06% and 29.40%, respectively.
Humans ; Asteraceae/chemistry* ; MCF-7 Cells ; Magnetic Resonance Spectroscopy ; Chromatography, High Pressure Liquid ; A549 Cells

PURPOSE: Tamoxifen has been well known as an effective anti-tumor agent against breast cancer. The important role of bcl-2 and p53 proteins in tamoxifen-induced apoptosis of breast cancer cells has been suggested. However, the paradoxical fact that bcl-2 over-expression is assdegrees Ciated with better prognosis in clinic has not yet been clearly explained. To investigate this paradox, we analyzed the effect and dynamics of bcl-2 and p53 on the apoptosis after treatment of breast cancer cells with tamoxifen. MATERIALS AND METHODS: The human breast cancer cell lines MCF-7 and MB MDA-468 were treated with 17-betaestradiol (E2) and tamoxifen. RESULTS: Following tamoxifen treatment, MCF-7 cells underwent apoptosis accompanied by reduced bcl-2 expression. E2 pre-treatment led to the inhibition of tamoxifen-mediated apoptosis and bcl-2 down-regulation. When MB MDA-468 cells were treated with E2 or tamoxifen, bcl-2 and p53 protein expression did not change and apoptosis did not develop. CONCLUSION: We observed that the down-regulation of bcl-2 by tamoxifen treatment can facilitate the apoptosis of breast cancer cells without p53 mutations. This finding was consistent with clinical experiences in which bcl-2 positive tumors were assdegrees Ciated with more indolent phenotypes in breast cancer.
Apoptosis* ; Breast Neoplasms* ; Breast* ; Cell Line* ; Down-Regulation ; Humans* ; MCF-7 Cells ; Phenotype ; Prognosis ; Tamoxifen

PURPOSE: To investigate the modulation of radiosensitivity by celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on cancer cells over- and under-expressing COX-2. MATERIALS AND METHODS: A clonogenic radiation survival analysis was performed on A549 human lung and MCF-7 human breast cancer cell lines incubated in both 1 and 10% fetal bovine serum (FBS) containing media. The apoptosis in both cell lines was measured after treatment with radiation and/or celecoxib. RESULTS: Celecoxib enhanced the radiation sensitivity of the A549 cells in the medium containing the 10% FBS, with radiation enhancement ratios of 1.58 and 1.81 respectively, at surviving fractions of 0.1, with 30 microM and 50 microM celecoxib. This enhanced radiosensitivity disappeared in the medium containing the 1% FBS. Celecoxib did not change the radiation sensitivity of the MCF-7 cells in either media. The induction of apoptosis by celecoxib and radiation was not synergistic in either cell line. CONCLUSION: Celecoxib, a selective COX-2 inhibitor, preferentially enhanced the effect of radiation on COX-2 over-expressing cancer cells compared to the cells with a low expression, and this effect disappeared on incubation of the cells during drug treatment in the medium with suboptimal serum concentration. Apoptosis did not appear to be the underlying mechanism of this radiation enhancement effect due to celecoxib on the A549 cells. These findings suggest radiosensitization by a selective COX-2 inhibitor is COX-2 dependent.
Apoptosis ; Breast Neoplasms ; Cell Line ; Cyclooxygenase 2* ; Humans* ; Lung ; MCF-7 Cells ; Radiation Tolerance* ; Celecoxib