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hypericin/καρκίνος του μαστού
Ο σύνδεσμος αποθηκεύεται στο πρόχειρο
Σελίδα 1 από 22 Αποτελέσματα
Down-regulation of Bcl-2 and Akt induced by combination of photoactivated hypericin and genistein in human breast cancer cells.
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Σύνδεση εγγραφή
Presented experiment considers combination of genistein and photodynamic therapy with hypericin with a view to achieve higher therapeutic outcome in human breast adenocarcinoma cell lines MCF-7 and MDA-MB-231, both identified in our conditions as photodynamic therapy resistant. Since genistein is
Effect of hypericin on the ADAMTS-9 and ADAMTS-8 gene expression in MCF7 breast cancer cells.
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OBJECTIVE
To investigate the effects of hypericin which is obtained from the plant Hypericum perforatum on the expression and the regulation of ADAMTS8 and ADAMTS9 genes in MCF7 breast cancer cells and on the viability of these cells.
METHODS
MCF7 cells were cultured and were separately exposed to
The effects of hypericin on ADAMTS and p53 gene expression in MCF-7 breast cancer cells.
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OBJECTIVE
The purpose of this study was to determine the effects of hypericin on MCF-7 (Michigan Cancer Foundation- 7) breast cancer cells, as it is known to exert an antitumor effect on the expression and regulation of ADAMTS1, 3, 10 and the p53 gene in breast cancer cells.
METHODS
MFC-7 cells were
Hypericin targets osteoclast and prevents breast cancer-induced bone metastasis via NFATc1 signaling pathway.
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Σύνδεση εγγραφή
Bone is the most common target organ of metastasis of breast cancers. This produces considerable morbidity due to skeletal-related events, and severely reduces the quality of life. Increased osteoclast activity is implicated in breast cancer outgrowth in the bone microenvironment. Our previous
Breast cancer resistance protein is the enemy of hypericin accumulation and toxicity of hypericin-mediated photodynamic therapy.
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Breast cancer resistance protein (BCRP) belongs to the family of ATP-binding cassette (ABC) transporters, overexpression of which can confer a multidrug-resistant phenotype in cancer cells and tumors. BCRP mediates efflux of numerous xenobiotics, including various chemotherapeutic agents and
Cytotoxic and apoptogenic effect of hypericin, the bioactive component of Hypericum perforatum on the MCF-7 human breast cancer cell line.
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BACKGROUND
Breast cancer is the most prevalent malignancies among the women that have a high mortality. Previous studies demonstrated that hypericin, a bioactive component of Hypericum perforatum have a cytotoxic effect on the malignant cell lines. However, an anti-carcinogenic activity of hypericin
Selective photodynamic effects on breast cancer cells provided by P123 Pluronic®-based nanoparticles modulating hypericin delivery.
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BACKGROUND
Breast cancer is the most relevant kind of cancer and the second cause of cancer- related deaths among women in general. Currently, there is no effective treatment for breast cancer although advances in its initial diagnosis and treatment available. Therefore, the value of novel
Correction: Hypericin targets osteoclast and prevents breast cancer-induced bone metastasis via NFATc1 signaling pathway.
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[This corrects the article DOI: 10.18632/oncotarget.22930.].
Hypericin and 5-aminolevulinic acid-induced protoporphyrin IX induce enhanced phototoxicity in human endometrial cancer cells with non-coherent white light.
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BACKGROUND
The in vitro experiments described in this study were aimed at exploring a synergistic effect between 5-aminolevulinic acid (5-ALA) induced protoporphyrin IX (PpIX) and hypericin. In a previous study, enhanced phototoxicity was observed in a patient during a clinical study on 5-ALA-based
Evaluation of the therapeutic efficacy of sequential therapy involving percutaneous microwave ablation in combination with 131I-hypericin using the VX2 rabbit breast solid tumor model.
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OBJECTIVE
Combination of percutaneous microwave ablation (PMWA) and intravenous injection of 131I-hypericin(IIIH) may bear potential as a mini-invasive treatment for tumor. The objective of this study was to assess the effect of PMWA and IIIH in breast tumor growth.
METHODS
Ten New Zealand White
Photoactivated hypericin induces downregulation of HER2 gene expression.
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Σύνδεση εγγραφή
Photodynamic therapy is an alternative method for cancer treatment in which a photosensitizer exposed to a light source of suitable wavelength is excited and can subsequently react through free radical mechanisms. Recently, oxygen free radical-mediated changes in gene expression have been
Degradation of HER2 receptor through hypericin-mediated photodynamic therapy.
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Σύνδεση εγγραφή
Current treatment of breast cancer is often affected by resistance to therapeutics, for which the human epidermal growth factor receptor 2 (HER2) may be responsible. Here, we report for the first time the use of hypericin-mediated photodynamic therapy (HY-PDT) in combination with a selective HER2
Drug membrane transporters and CYP3A4 are affected by hypericin, hyperforin or aristoforin in colon adenocarcinoma cells.
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Σύνδεση εγγραφή
Our previous results have shown that the combination of hypericin-mediated photodynamic therapy (HY-PDT) at sub-optimal dose with hyperforin (HP) (compounds of Hypericum sp.), or its stable derivative aristoforin (AR) stimulates generation of reactive oxygen species (ROS) leading to antitumour
Hypericin Induces Apoptosis in MDA-MB-175-VII Cells in Lower Dose Compared to MDA-MB-231.
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BACKGROUND
Breast cancer is the major cause of death from cancer among women around the world. Given the drug resistance in the treatment of this disease, it is very important to identify new therapies and anticancer drugs. Many studies demonstrated that hypericin could induce apoptosis in different
Single pre-treatment with hypericin, a St. John's wort secondary metabolite, attenuates cisplatin- and mitoxantrone-induced cell death in A2780, A2780cis and HL-60 cells.
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Σύνδεση εγγραφή
St. John's wort (SJW, Hypericum perforatum L.) is a commonly used natural antidepressant responsible for the altered toxicity of some anticancer agents. These interactions have been primarily attributed to the hyperforin-mediated induction of some pharmacokinetic mechanisms. However, as previously
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