withania somnifera/emlőrák

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Withaferin A suppresses breast cancer cell proliferation by inhibition of the two-pore domain potassium (K2P9) channel TASK-3

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Withaferin A (WFA), a C₅,C₆-epoxy steroidal lactone isolated from the medicinal plant Withania somnifera (L.) Dunal, inhibits growth of tumor cells in different cancer types. However, the mechanisms underlying the effect of WFA on tumor cells are not fully understood. In the

In silico elucidation of plausible inhibitory potential of Withaferin A of Withania somnifera medicinal herb against breast cancer targeting estrogen receptor.

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Estrogen receptors (ER) are members of the nuclear intracellular receptors family. ER once activated by estrogen, it binds to DNA via translocating into the nucleus and regulates the activity of various genes. In about one third of the breast cancer cases, ERs are over expressed and this condition

Withania somnifera extract reduces the invasiveness of MDA-MB-231 breast cancer and inhibits cytokines associated with metastasis.

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OBJECTIVE The aim was to examine the anti-proliferative effect of a Withania somnifera (WS) root extract in cell cultures and nude mouse xenografts of breast cancer cell line MDA-MB-231. METHODS WS root extract was used to treat tumor cells at concentrations up to 100 µg and for nude mouse

Evaluation of apoptotic activity of Withania coagulans methanolic extract against human breast cancer and Vero cell lines.

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BACKGROUND The genus Withania (Family: Solanaceae) holds an important position in Ayurveda, the Indian traditional system of medicine. Withania somnifera Dunal and Withania coagulans Dunal have been documented in folklore as panaceas for various ailments since time immemorial. W. coagulans (WC),

Synthesis, Characterization and Anti-Cancer Therapeutic Potential of Withanolide-A with 20nm sAuNPs Conjugates Against SKBR3 Breast Cancer Cell Line

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Background: Nanotechnology is gaining emerging interest in advanced drug discovery therapeutics due to their tremendous properties including enhanced delivery of therapeutic payload, extensive surface to volume ratio, high permeability,

Withaferin a suppresses estrogen receptor-α expression in human breast cancer cells.

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We have shown previously that withaferin A (WA), a promising anticancer constituent of Ayurvedic medicine plant Withania somnifera, inhibits growth of MCF-7 and MDA-MB-231 human breast cancer cells in culture and MDA-MB-231 xenografts in vivo by causing apoptosis. However, the mechanism of

Withaferin A inhibits activation of signal transducer and activator of transcription 3 in human breast cancer cells.

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We have shown previously that withaferin A (WA), a promising anticancer constituent of Ayurvedic medicine plant Withania somnifera, inhibits growth of human breast cancer cells in culture and in vivo in association with apoptosis induction. The present study builds on these observations and

Molecular docking, QSAR and ADMET studies of withanolide analogs against breast cancer.

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Withanolides are a group of pharmacologically active compounds present in most prodigal amounts in roots and leaves of Withania somnifera (Indian ginseng), one of the most important medicinal plants of Indian traditional practice of medicine. Withanolides are steroidal lactones (highly oxygenated

Withaferin A inhibits expression of ataxia telangiectasia and Rad3-related kinase and enhances sensitivity of human breast cancer cells to cisplatin.

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Ataxia telangiectasia and Rad3-related (ATR) is a serine/threonine-specific kinase that plays an important role in the maintenance of genomic integrity. In this study, we investigated the role of ATR in cell-cycle arrest by withaferin A (WA), a cancer preventative steroidal lactone derived from

A comprehensive review and perspective on anticancer mechanisms of withaferin A in breast cancer

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Withaferin A (hereafter abbreviated as WA) is a promising anticancer steroidal lactone abundant in a medicinal plant (Withania somnifera) native to Asia. The root/leaf extract of Withania somnifera, which belongs to the Solanaceae family, continues to be included in the Ayurvedic medicine

Withaferin A induced impaired autophagy and unfolded protein response in human breast cancer cell-lines MCF-7 and MDA-MB-231.

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The autophagy-lysosome pathway and the ubiquitin-proteasome systems are the two major routes for eukaryotic intracellular protein clearance. Cancerous cells often display elevated protein synthesis and byproduct disposal, thus, inhibition of the protein degradation pathways became an emerging

Ayurvedic medicine constituent withaferin a causes G2 and M phase cell cycle arrest in human breast cancer cells.

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Withaferin A (WA) is derived from the medicinal plant Withania somnifera that has been safely used for centuries in the Indian Ayurvedic medicine for treatment of various ailments. We now demonstrate that WA treatment causes G2 and mitotic arrest in human breast cancer cells. Treatment of MDA-MB-231

Withaferin A-induced apoptosis in human breast cancer cells is associated with suppression of inhibitor of apoptosis family protein expression.

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The present study provides novel insight into the mechanism of apoptosis induction by withaferin A (WA), which is a bioactive constituent of an Ayurvedic medicine plant (Withania somnifera). Exposure of MDA-MB-231 and MCF-7 human breast cancer cells to WA resulted in suppression of XIAP, cIAP-2, and

Withaferin A causes FOXO3a- and Bim-dependent apoptosis and inhibits growth of human breast cancer cells in vivo.

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Withaferin A (WA) is derived from the medicinal plant Withania somnifera, which has been safely used for centuries in Indian Ayurvedic medicine for treatment of different ailments. We now show, for the first time, that WA exhibits significant activity against human breast cancer cells in culture and

Withaferin A causes activation of Notch2 and Notch4 in human breast cancer cells.

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Ayurvedic medicine plants continue to draw attention for the discovery of novel anticancer agents. Withaferin A (WA) is one such small-molecule constituent of the ayurvedic medicine plant Withania somnifera with efficacy against cultured and xenografted human breast cancer cells. However, the

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