tripterygium wilfordii/rinnavähk

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Celastrol induces the apoptosis of breast cancer cells and inhibits their invasion via downregulation of MMP-9.

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Celastrol is a quinone methide triterpene derived from Tripterygium wilfordii Hook F., a plant used in traditional medicine. In the present study, we reported that celastrol potentiated tumor necrosis factor-α (TNF-α)-induced apoptosis, affected activation of caspase-8, caspase-3 and PARP cleavage,

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

Celastrol Inhibits Migration and Invasion of Triple-Negative Breast Cancer Cells by Suppressing Interleukin-6 via Downregulating Nuclear Factor-κB (NF-κB)

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BACKGROUND Celastrol is extracted from the root of the Chinese traditional herb Tripterygium wilfordii, which has anti-cancer effects in multiple cancers. However, the effect of celastrol on the metastasis of triple-negative breast cancer and its mechanism remain largely unknown. MATERIAL AND

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

Demethylzeylasteral (T-96) inhibits triple-negative breast cancer invasion by blocking the canonical and non-canonical TGF-β signaling pathways.

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Inflammation is one of the characteristic features during the development of human tumors. A pro-inflammatory cytokine that is known to promote inflammation during cancer development is the transforming growth factor-β (TGF-β). On the other hand, demethylzeylasteral (T-96) is a natural compound

Preparation of high drug-loading celastrol nanosuspensions and their anti-breast cancer activities in vitro and in vivo

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As one of the main components of Tripterygium wilfordii Hook F, celastrol (CSL) has significant antitumor activity, but its clinical application has been limited by its poor solubility, low oral bioavailability and systemic toxicity. In this study, celastrol nanosuspensions (CSL-NSps) were prepared

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 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

Triptolide inhibits interferon-gamma-induced programmed death-1-ligand 1 surface expression in breast cancer cells.

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Triptolide, a natural compound purified from the Chinese herb Tripterygium wilfordii, has been reported to inhibit the growth and metastasis of tumors in vivo. However, the effects of triptolide on the immune responses of cancer cells remain unknown. Up-regulation of programmed death-1-ligand 1

Triptolide sensitizes breast cancer cells to Doxorubicin through the DNA damage response inhibition.

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Triptolide is an active component from a Chinese herb, Tripterygium wilfordii which has been applied for treating immune-related diseases over centuries. Recently, it was reported that a variety of cancer cell lines could be sensitized to DNA-damage based chemotherapy drugs in combination with

Celastrol induces ubiquitin-dependent degradation of mTOR in breast cancer cells.

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Background

Celastrol is a major active component of the thunder god vine (Tripterygium wilfordii) used in traditional Chinese medicine to treat chronic inflammatory and autoimmune diseases. Celastrol inhibits PI3K-Akt-mTOR signaling, which is frequently dysregulated in

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