triptolide/karcinom prsu

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Effects of triptolide from Tripterygium wilfordii on ERalpha and p53 expression in two human breast cancer cell lines.

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The aim of the study was to discover possible differential cytotoxicity of triptolide towards estrogen-sensitive MCF-7 versus estrogen-insensitive MDA-MB-231 human breast cancer cells. Considering that MCF-7 cells express functional Estrogen receptor alpha (ERalpha) and wild-type p53, whereas

Antiestrogenic Activity of Triptolide in Human Breast Cancer Cells MCF-7 and Immature Female Mouse.

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Preclinical Research To investigate the antiestrogenic activity of triptolide in human breast cancer cell line MCF-7 and immature female C57BL/6 mouse. The effects of triptolide on cell proliferation, cell cycle, and the expression of estrogen receptor alpha (ERα) and progesterone receptor (PR) were

Triptolide interferes with XRCC1/PARP1-mediated DNA repair and confers sensitization of triple-negative breast cancer cells to cisplatin.

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Triptolide is a natural compound isolated from the Tripterygium wilfordii, which possesses anti-inflammatory and anti-tumor activities. Triptolide reportedly inhibits RNA polymerase II-mediated transcription and ATM activities to interfere with DNA repair. However, the roles of triptolide in DNA

Molecularly Engineer Triptolide with Aptamers for High Specifici-ty and Cytotoxicity for Triple-Negative Breast Cancer.

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Triple-negative breast cancer (TNBC) lacks three important recep-tors (ER, PR, and HER2), and thus has been identified as one of the most malignant cancer types. The development of efficient tar-geted TNBC therapy has been considered as an important research topic in TNBC treatment. We report the

Triptolide has anticancer and chemosensitization effects by down-regulating Akt activation through the MDM2/REST pathway in human breast cancer.

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Triptolide has been shown to exhibit anticancer activity. However, its mechanism of action is not clearly defined. Herein we report a novel signaling pathway, MDM2/Akt, is involved in the anticancer mechanism of triptolide. We observed that triptolide inhibits MDM2 expression in human breast cancer

Inhibition of insulin-like growth factor 1 signaling synergistically enhances the tumor suppressive role of triptolide in triple-negative breast cancer cells.

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Triptolide (TPL) is an active extract from a Chinese herb, which has been used for centuries in China. TPL exhibits numerous bioactivities and pharmacological effects, including antitumor, anti-inflammatory and immunosuppressive activities. However, previous studies have further revealed a

Does triptolide induce lysosomal-mediated apoptosis in human breast cancer cells?

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With breast cancer plaguing the United States as the second leading cause of cancer related deaths amongst women, as well as the adverse effects of current treatment options there is a need to develop safer and noninvasive treatments. Triptolide is an extract from the herb Tripterygium wilfordii

Triptolide induces lysosomal-mediated programmed cell death in MCF-7 breast cancer cells.

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BACKGROUND Breast cancer is a major cause of death; in fact, it is the most common type, in order of the number of global deaths, of cancer in women worldwide. This research seeks to investigate how triptolide, an extract from the Chinese herb Tripterygium wilfordii Hook F, induces apoptosis in

Effect of triptolide on focal adhesion kinase and survival in MCF-7 breast cancer cells.

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Triptolide, a diterpene from Tripterygium wilfordii, has been shown to have potent anticancer activity, exerting its effects through multiple molecular targets and signaling pathways. Yet, its effect on focal adhesion kinase (FAK), a non-receptor tyrosine kinase overexpressed in breast cancer that

Triptolide Decreases Cell Proliferation and Induces Cell Death in Triple Negative MDA-MB-231 Breast Cancer Cells.

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Triple negative breast cancers (TNBCs) do not respond to conventional estrogen receptor/progesterone receptor/human epidermal growth factor receptor-2 targeted interventions due to the absence of the respective receptor targets. They are aggressive, exhibit early recurrence, metastasize, are more

Triptolide-induced in vitro and in vivo cytotoxicity in human breast cancer stem cells and primary breast cancer cells.

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We investigated the potential efficacy of the Chinese herbal extract triptolide for the treatment of human breast cancer by measuring the triptolide-induced cytotoxicity in cultures of human primary breast cancer cells (BCCs) and breast cancer stem cells (BCSCs) in vitro and in vivo. Human BCCs and

Triptolide sensitizes human breast cancer cells to tumor necrosis factor‑α‑induced apoptosis by inhibiting activation of the nuclear factor‑κB pathway.

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Tumor necrosis factor‑α (TNF‑α) can act as either a tumor promoter, linking inflammation with carcinogenesis, or a tumor inhibitor, inducing cancer cell death. However, several types of cancer, including breast cancer, are resistant to TNF‑α therapy. Triptolide, a diterpene triepoxide, has been

Triptolide inhibits human breast cancer MCF-7 cell growth via downregulation of the ERα-mediated signaling pathway.

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OBJECTIVE To investigate the anticancer mechanisms of triptolide, a diterpenoid isolated from the plant Tripterygium wilfordii Hook F, against human breast cancer cells and the involvement of the estrogen receptor-α (ERα)-mediated signaling pathway in particular. METHODS Human breast cancer

Triptolide-loaded nanoparticles targeting breast cancer in vivo with reduced toxicity.

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Triptolide (TP), a diterpenoid triepoxide that is extracted from the plant Tripterygium wilfordii, has been found to be quite effective for treating many malignant tumors. Although TP was initially considered to be a promising chemotherapeutic agent, its poor solubility and high toxicity limited its

Triptolide Inhibits Breast Cancer Cell Metastasis Through Inducing the Expression of miR-146a, a Negative Regulator of Rho GTPase.

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Triptolide, an extract of Tripterygium wilfordii, has been shown to have a potent anticancer activity. In the present study, it was found that triptolide could effectively induce apoptosis and inhibit proliferation and invasion in malignant MDA-MB-231 breast cancer cells. The study focused on

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