acteoside and Breast-Neoplasms

acteoside has been researched along with Breast-Neoplasms* in 3 studies

Other Studies

3 other study(ies) available for acteoside and Breast-Neoplasms

ArticleYear
The cytotoxicity and apoptotic effects of verbascoside on breast cancer 4T1 cell line.
    BMC pharmacology & toxicology, 2021, 11-29, Volume: 22, Issue:1

    Despite significant advancements in breast cancer therapy, novel drugs with lower side effects are still being demanded. In this regard, we investigated the anti-cancer features of verbascoside in 4 T1 mouse mammary tumor cell.. First, MTT assay was performed with various concentrations (ranging between 5 to 200 μM) of verbascoside and IC50 was calculated. Then the expression of Bax, Bcl-2, and caspase-3 was evaluated in treated 4 T1 cells. In addition, we investigated the expression of TLR4, MyD88, and NF-κB to ascertain the underlying mechanism of the anti-proliferative feature of verbascoside. Also, flow cytometry followed by double PI and Annexin V was conducted to confirm the apoptosis-inducing effect of verbascoside.. Our results from MTT assay showed verbascoside inhibits proliferation of 4 T1 cancer cells (IC50 117 μM) while is safe for normal HEK293T cells. By qRT-PCR, we observed that verbascoside treatment (100, 117 and, 130 μM) increases the expression of caspase-3 and Bax while reduces the expression of Bcl-2. Also, verbascoside (100, 117 and, 130 μM) increased the expression of TLR4 only at 130 μM dose and the expression of MyD88 whereas reduced the expression of NF-κB at mRNA level. Flow cytometry analysis also confirmed verbascoside induces apoptosis in 4 T1 cells at 117 μM.. Taken together, our data showed verbascoside is a safe natural compound for normal cells while has apoptosis-inducing feature through TLR4 axis on 4 T1 cells.

    Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Breast Neoplasms; Caspase 3; Cell Line; Cell Proliferation; Cell Survival; Gene Expression Regulation, Neoplastic; Glucosides; Humans; Mice; Myeloid Differentiation Factor 88; NF-kappa B; Phenols; Proto-Oncogene Proteins c-bcl-2; Toll-Like Receptor 4

2021
A metabolite-profiling approach to assess the uptake and metabolism of phenolic compounds from olive leaves in SKBR3 cells by HPLC-ESI-QTOF-MS.
    Journal of pharmaceutical and biomedical analysis, 2013, Volume: 72

    Olive leaves, an easily available natural low-cost material, constitute a source of extracts with significant antitumor activity that inhibits cell proliferation in several breast-cancer-cell models. In this work, a metabolite-profiling approach has been used to assess the uptake and metabolism of phenolic compounds from an olive-leaf extract in the breast-cancer-cell line SKBR3 to evaluate the compound or compounds responsible for the cytotoxic activity. For this, the extract was firstly characterized quantitatively by high-performance liquid chromatography coupled to electrospray ionization-quadrupole time-of-flight mass spectrometry (HPLC-ESI-QTOF-MS). Then, SKBR3 cells were incubated with 200 μg/mL of the olive-leaf extract at different times (15 min, 1, 2, 24, and 48 h). A metabolite-profiling approach based on HPLC-ESI-QTOF-MS was used to determine the intracellular phenolic compounds, enabling the identification of 16 intact phenolic compounds from the extract and four metabolites derived from these compounds in the cell cytoplasm. The major compounds found within the cells were oleuropein, luteolin-7-O-glucoside and its metabolites luteolin aglycone and methyl-luteolin glucoside, as well as apigenin, and verbascoside. Neither hydroxytyrosol nor any of its metabolites were found within the cells at any incubation time. It is proposed that the major compounds responsible for the cytotoxic activity of the olive-leaf extract in SKBR3 cells are oleuropein and the flavones luteolin and apigenin, since these compounds showed high uptake and their antitumor activity has been previously reported.

    Topics: Apigenin; Breast Neoplasms; Carcinoma; Cell Line, Tumor; Chromatography, High Pressure Liquid; Cytoplasm; Female; Flavones; Glucosides; Humans; Iridoid Glucosides; Iridoids; Luteolin; Olea; Phenols; Plant Extracts; Plant Leaves; Pyrans; Spectrometry, Mass, Electrospray Ionization; Tandem Mass Spectrometry

2013
Acteoside and martynoside exhibit estrogenic/antiestrogenic properties.
    The Journal of steroid biochemistry and molecular biology, 2006, Volume: 98, Issue:1

    Acteoside and martynoside are plant phenylpropanoid glycosides exhibiting anticancer, cytotoxic and antimetastatic activities. We investigated their potential to activate estrogen receptor isoforms ERalpha and ERbeta in HeLa cells transfected with an estrogen response element (ERE)-driven luciferase (Luc) reporter gene and an ERalpha or ERbeta expression vector. Their estrogenic/antiestrogenic effects were also assessed in breast cancer cells (MCF7), endometrial cancer cells (Ishikawa) and osteoblasts (KS483), by measuring IGFBP3 levels, cell viability and number of mineralized nodules, respectively, seeking for a natural selective estrogen receptor modulator (SERM). Acteoside and martynoside antagonized both ERalpha and ERbeta (p<0.001), whereas they reversed the effect of E(2) mainly via ERalpha (p<0.001). Martynoside was a potent antiestrogen in MCF-7 cells, increasing, like ICI182780, IGFBP3 levels via the ER-pathway. In osteoblasts, martynoside induced nodule mineralization, which was abolished by ICI182780, implicating an ER-mediated mechanism. Furthermore, its antiproliferative effect on endometrial cells suggests that martynoside may be an important natural SERM. Acteoside was an antiestrogen in breast cancer cells and osteoblasts, without any effect on endometrial cells. Our study suggests that the nature is rich in selective ERalpha and ERbeta ligands, the discovery of which may lead to the development of novel neutraceutical agents.

    Topics: Breast Neoplasms; Calcinosis; Cell Survival; Endometrial Neoplasms; Estradiol Congeners; Estrogen Antagonists; Estrogen Receptor alpha; Estrogen Receptor beta; Female; Glucosides; HeLa Cells; Humans; Insulin-Like Growth Factor Binding Protein 3; Ligands; Osteoblasts; Phenols; Response Elements; Selective Estrogen Receptor Modulators; Transfection; Tumor Cells, Cultured

2006