trichosanthin/neoplasms

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Trichosanthin inhibits DNA methyltransferase and restores methylation-silenced gene expression in human cervical cancer cells.

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Epigenetic silencing of tumor suppressor genes is a well-established oncogenic process and the reactivation of tumor suppressor genes that have been silenced by promoter methylation is an attractive molecular target for cancer therapy. In this study, we investigated the demethylation activity of

Trichosanthin inhibits breast cancer cell proliferation in both cell lines and nude mice by promotion of apoptosis.

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Breast cancer ranks as a common and severe neoplasia in women with increasing incidence as well as high risk of metastasis and relapse. Translational and laboratory-based clinical investigations of new/novel drugs are in progress. Medicinal plants are rich sources of biologically active natural

Smac is another pathway in the anti-tumour activity of Trichosanthin and reverses Trichosanthin resistance in CaSki cervical cancer cells.

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Trichosanthin (TCS), or Tin Hua Fen, is a renowned traditional Chinese medicine and is still used in Chinese clinics for midterm abortion and the treatment of choriocarcinoma. Many studies have demonstrated that TCS has anti-tumour action as a type I ribosome-inactivating protein. We hypothesized

Enhanced anti-tumor activity of trichosanthin after combination with a human-derived cell-penetrating peptide, and a possible mechanism of activity.

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Trichosanthin (TCS), a type I ribosome-inactivating protein (RIP-I) and renowned Chinese traditional medicine, displays a broad spectrum of biological and pharmacological properties. Particularly, its anti-tumor activity has received a great deal of attention. However, the cellular mechanism for TCS

Trichosanthin enhances anti-tumor immune response in a murine Lewis lung cancer model by boosting the interaction between TSLC1 and CRTAM.

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Trichosanthin (TCS), extracted from the Chinese medicinal herb Trichosanthes kirilowi, has shown promise for the inhibition of tumor growth. However, its immunomodulatory effect on tumor-host interaction remains unknown. In this study, we focused on the effect of TCS on murine anti-tumor immune

Possible mechanisms of trichosanthin-induced apoptosis of tumor cells.

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Trichosanthin (TCS) is a type I ribosome-inactivating protein that is isolated from the root tubers of the Chinese medicinal herb Trichosanthes kirilowii Maximowicz. TCS has been used as an abortifacient for 1,500 years in China because of its high toxicity on trophoblasts. Over the past 20 years,

The anti-cancerous activity of recombinant trichosanthin on prostate cancer cell PC3.

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BACKGROUND Trichosanthin produced in the root tube of Trichosanthes kirilowii shows anti-tumor activity on a series of cancer cells including Hela, MCF-7, HL-60. But there is little information about its effect on the carcinogenesis of prostate cancer. OBJECTIVE This work was designed to study the

A novel trichosanthin fusion protein with increased cytotoxicity to tumor cells.

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OBJECTIVE To evaluate the anti-tumor effects of trichosanthin after fusion with a cell penetrating peptide, heparin-binding peptide (HBP), derived from human heparin-binding EGF-like growth factor (HB-EGF). RESULTS The fusion protein of trichosanthin-HBP was expressed in Escherichia coli BL21 and

Toxicities of trichosanthin and alpha-momorcharin, abortifacient proteins from Chinese medicinal plants, on cultured tumor cell lines.

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Trichosanthin and alpha-momorcharin are abortifacient proteins extracted from Chinese medicinal herbs. Study of their in vitro cytotoxicities showed that the two proteins selectively injured choriocarcinoma and melanoma cells. Hepatoma cells represented the most resistant cell line among the various

Trichosanthin inhibits the proliferation of cervical cancer cells and downregulates STAT-5/C-myc signaling pathway.

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Previous studies have indicated that Trichosanthin (TCS) exerts anti-virus, immunoregulation and a broad spectrum anti-tumor pharmacological activities. Trichosanthin is a promising agent for the treatment of cervical cancer. However, the exact effects and potential mechanism of TCS on

Trichosanthin enhances sensitivity of non-small cell lung cancer (NSCLC) TRAIL-resistance cells.

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Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) has a specific antitumour activity against many malignant tumours. However, more than half of lung cancer cells are resistant to TRAIL-relevant drugs. Trichosanthin (TCS) is a traditional Chinese medicine with strong inhibitive effects

Trichosanthin enhances the antitumor effect of gemcitabine in non-small cell lung cancer via inhibition of the PI3K/AKT pathway.

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Gemcitabine (GEMZ) is the first-line therapy used against non-small cell lung cancer (NSCLC), and studies have focused on investigating the potential effects of agents combined with GEMZ to enhance the anticancer efficacy in NSCLC. Previous studies have reported that trichosanthin (TCS) has various

Trichosanthin increases Granzyme B penetration into tumor cells by upregulation of CI-MPR on the cell surface.

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Trichosanthin is a plant toxin belonging to the family of ribosome-inactivating proteins. It has various biological and pharmacological activities, including anti-tumor and immunoregulatory effects. In this study, we explored the potential medicinal applications of trichosanthin in cancer

Trichosanthin-induced autophagy in gastric cancer cell MKN-45 is dependent on reactive oxygen species (ROS) and NF-κB/p53 pathway.

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Trichosanthin (TCS), isolated from the root tuber of Trichosanthes kirilowii tubers in the Cucurbitaceae family, owns a great deal of biological and pharmacological activities including anti-virus and anti-tumor. TCS has been reported to induce cell apoptosis of a diversity of cancers, including

Co-Delivery of Trichosanthin and Albendazole by Nano-Self-Assembly for Overcoming Tumor Multidrug-Resistance and Metastasis.

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Multidrug resistance (MDR) and metastasis are the major obstacles in cancer chemotherapy. Nanotechnology-based combination therapy is a useful strategy. Recently, the combination of biologics and small drugs has attracted much attention in cancer therapy. Yet, the treatment outcomes are often

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