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resveratrol/sarkom
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Reverse chemomodulatory effects of the SIRT1 activators resveratrol and SRT1720 in Ewing's sarcoma cells: resveratrol suppresses and SRT1720 enhances etoposide- and vincristine-induced anticancer activity.
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OBJECTIVE
SIRT1-activating compounds (STACs) may have potential in the management of cancer. However, the best-studied STAC, the naturally occurring compound resveratrol, is reported to have contradictory effects in combination chemotherapy regimens: It has been shown both to increase and to
The growth of the canine glioblastoma cell line D-GBM and the canine histiocytic sarcoma cell line DH82 is inhibited by the resveratrol oligomers hopeaphenol and r2-viniferin.
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Vineatrol(®) 30 is a grapevine-shoot extract, which contains resveratrol as well as considerable amounts of so-called resveratrol oligomers such as hopeaphenol and r2-viniferin. In this study, we analysed whether the two above-mentioned resveratrol oligomers were able to inhibit the growth of the
Resveratrol suppresses proliferation and induces apoptosis of uterine sarcoma cells by inhibiting the Wnt signaling pathway.
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Resveratrol, a natural product and peroxisome proliferator-activated receptor (PPAR) agonist, has been reported to exert anti-cancer effects in several tumor models. A previous study by our group reported that prostaglandin J2, a PPARγ ligand, inhibited cell proliferation in a uterine sarcoma cell
Resveratrol and diallyl disulfide enhance curcumin-induced sarcoma cell apoptosis.
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Malignant tumors of mesenchimal origin such as rhabdomyosarcoma and osteosarcoma are highly aggressive pedriatic malignancies with a poor prognosis. Indeed, the initial response to chemotherapy is followed by chemoresistance. Diallyl disulfide (DADS), resveratrol (RES) and curcumin (CUR) are dietary
Antitumor activity of resveratrol against human osteosarcoma cells: a key role of Cx43 and Wnt/β-catenin signaling pathway.
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Osteosarcoma is a high-grade bone sarcoma with strong invasive ability. However, treatment with traditional chemotherapeutic drugs is limited by low tolerability and side effects. Resveratrol has been reported previously to have selective antitumor effect on various tumor cells while little is known
Inhibitory Effects of Resveratrol on the Human Alveolar Rhabdomyosarcoma Cell Line PLA-802 through Inhibition of the TGF-β1/Smad Signaling Pathway.
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While anti-tumor activity of resveratrol has been demonstrated for many cancers, little is known about its effects on soft tissue sarcoma. Overexpression of TGF-β1, a protein inhibited by resveratrol, is a well-known feature of the rhabdomyosarcoma (RMS), a type of soft tissue sarcoma. In the
Relative effects of phenolic constituents from Yucca schidigera Roezl. bark on Kaposi's sarcoma cell proliferation, migration, and PAF synthesis.
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Yuccaols (A, B, C) are phenolic constituents isolated from Yucca schidigera bark characterized by unusual spirostructures made up of a C15 unit and a stilbenic portion closely related to resveratrol. These novel compounds are of particular interest for their antioxidant and anti-inflammatory
Antitumor effect of stilbenoids from Vateria indica against allografted sarcoma S-180 in animal model.
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Dipterocarpaceous plants contain various resveratrol oligomers that exhibit a variety of biological activities, such as antibacterial and antitumor effects. Previously, we found that vaticanol C, a resveratrol tetramer, exhibits strong cytotoxicity against various tumor cell lines. In the present
Resveratrol induces luminal apoptosis of human colorectal cancer HCT116 cells in three-dimensional culture.
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BACKGROUND
We have previously reported the crucial roles of oncogenic Kirsten rat sarcoma viral oncogene homolog (KRAS) in inhibiting apoptosis and disrupting cell polarity via the regulation of phosphodiesterase 4 (PDE4) expression in human colorectal cancer HCT116 cells in three-dimensional
Application of open-access databases to determine functional connectivity between resveratrol-binding protein QR2 and colorectal carcinoma.
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Colorectal cancer (CRC) is a major cause of cancer-associated deaths worldwide. Recently, oral administration of resveratrol (trans-3,5,4'-trihydroxystilbene) has been reported to significantly reduce tumor proliferation in colorectal cancer patients, however, with little specific information on
Resveratrol inhibits KSHV reactivation by lowering the levels of cellular EGR-1.
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In the field of herpesvirus research, the exact molecular mechanism by which such viruses reactivate from latency remains elusive. Kaposi's sarcoma-associated herpesvirus (KSHV) primarily exists in a latent state, while only 1-3% of cells support lytic infection at any specific time. KSHV
Resveratrol in management of bone and spinal cancers.
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Bone cancer is a malignant primary tumour of the bone with different typing, such as, osteosarcoma, chondrosarcoma, Ewing's sarcoma and fibrosarcoma. Despite the clinical efficacy of conventional therapies of bone cancer, most patients eventually relapse and the disease remains incurable. Therefore,
Ligand structure-dependent differences in activation of estrogen receptor alpha in human HepG2 liver and U2 osteogenic cancer cell lines.
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Differences in ligand-activation of estrogen receptor alpha (ER(alpha)) were investigated in human HepG2 liver carcinoma and U2 osteogenic sarcoma cells transfected with wild-type ER (ER-wt) and variants expressing only activation function 1 (ERAF1) or AF2 (ER-AF2). The estrogen-responsive C3-luc
Toxicology of environmental estrogens.
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It has been hypothesized that environmental contaminants that modulate endocrine signaling pathways may be causally linked to adverse health effects in humans. There has been particular concern regarding synthetic estrogens and their role in disrupting normal development of the male reproductive
Caffeic acid phenethyl ester (CAPE) prevents transformation of human cells by arsenite (As) and suppresses growth of As-transformed cells.
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Recent evidence suggests that inflammatory cytokines and growth factors contribute to arsenite (As)-induced human carcinogenesis. We investigated the expression of inflammatory cytokine mRNAs during the transformation process induced by chronic As exposure in non-tumorigenic human osteogenic sarcoma
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