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amentoflavone/neoplasms
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Sida 1 från 67 resultat
Amentoflavone Promotes Apoptosis in Non-small-cell Lung Cancer by Modulating Cancerous Inhibitor of PP2A.
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Non-small-cell lung cancer (NSCLC) is one of the most common human malignancies. Amentoflavone (AF) is one of bioflavonoid compounds isolated from Selaginella tamariscina Spring. This study was designed to examine the effect of AF on NSCLC. Our results indicated that AF decreased cell viability of
Fatty acid synthase inhibition by amentoflavone induces apoptosis and antiproliferation in human breast cancer cells.
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Fatty acid synthase (FASN) is highly expressed in breast carcinomas to support their continuous growth and proliferation, but has low expression level in normal tissues. Considerable interest has been developed in searching for novel FASN inhibitors as a therapeutic target for breast cancer. In
Fatty acid synthase inhibition by amentoflavone suppresses HER2/neu (erbB2) oncogene in SKBR3 human breast cancer cells.
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Fatty acid synthase (FASN) is a potential therapeutic target for treatment of cancer and obesity, and is highly elevated in 30% of HER2-overexpressing breast cancers. Considerable interest has developed in searching for novel FASN inhibitors as therapeutic agents in treatment of HER2-overexpressing
Amentoflavone Inhibits ERK-modulated Tumor Progression in Hepatocellular Carcinoma In Vitro.
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A previous study indicated that amentoflavone inhibits tumor growth of breast cancer. However, the anti-cancer effects and mechanism of amentoflavone in hepatocellular carcinoma (HCC) have not been elucidated. The aim of the present study was to verify the effect of amentoflavone on tumor
Amentoflavone stimulates apoptosis in B16F-10 melanoma cells by regulating bcl-2, p53 as well as caspase-3 genes and regulates the nitric oxide as well as proinflammatory cytokine production in B16F-10 melanoma cells, tumor associated macrophages and peritoneal macrophages.
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Polyphenolic compounds present in fruits, vegetables, herbs, roots and leaves act as bioactive components and has been recognized as cancer chemopreventive agents. The present study is focused on the regulatory effect of amentoflavone, a biflavonoid from Biophytum sensitivum on the apoptotic process
Inhibition of tumor specific angiogenesis by amentoflavone.
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The formation of new capillaries from existing blood vessels is critical for tumor growth and metastasis. In this study we report that amentoflavone, a biflavonoid from Biophytum sensitivum, could inhibit the process of angiogenesis. Amentoflavone at nontoxic concentrations (0.05-0.2 microg/ml)
The biflavonoid amentoflavone induces apoptosis via suppressing E7 expression, cell cycle arrest at sub-G₁ phase, and mitochondria-emanated intrinsic pathways in human cervical cancer cells.
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Amentoflavone, a biflavonoid from Selaginella tamariscina, is known to possess several bioactivities such as antitumor, anti-inflammatory, and antifungal effects. However, the mechanism of the anticancer effects of amentoflavone on human cervical cancer cells has not been studied in detail. In this
Identification of amentoflavone as a potent highly selective PARP-1 inhibitor and its potentiation on carboplatin in human non-small cell lung cancer.
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BACKGROUND
Nuclear protein poly (ADP-ribose) polymerase-1 (PARP-1) is a key enzyme in the repair of DNA and is a promising target in the development of chemosensitizers. This study first investigated the inhibitory effects of amentoflavone (AMF) and its derivatives on PARP-1 and the potentiation of
Amentoflavone, a biflavonoid from Biophytum sensitivum augments lymphocyte proliferation, natural killer cell and antibody dependent cellular cytotoxicity through enhanced production of IL-2 and IFN-gamma and restrains serum sialic acid and gamma glutamyl transpeptidase production in tumor - bearing animals.
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Modulation of immune response is highly relevant in tumor cell destruction. The present study is focused on the effect of amentoflavone, a biflavonoid from Biophytum sensitivum on cell-mediated immune responses in normal and tumor-bearing control animals. Tumor was induced in BALB/c mice by
Data on the anti-tumor effects of Selaginella tamariscina extract and amentoflavone combined with doxorubicin in mice.
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Here, we report animal experimental data associated with the article entitled "AKR1B10-inhibitory Selaginella tamariscina extract and amentoflavone decrease the growth of A549 human lung cancer cells in vitro and in vivo" (Jung et al., 2017) [1]. We tested the synergistic anti-tumor effects of
Amentoflavone, active compound of Selaginella tamariscina, inhibits in vitro and in vivo TGF-β-induced metastasis of human cancer cells.
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Epithelial mesenchymal transition (EMT) is a well-known and important step in metastasis and thus can be a key target in cancer treatment. Here, we tested the EMT inhibitory actions of Selaginella tamariscina and its active component, amentoflavone (AF). EMT was examined in vitro using wound-healing
AKR1B10-inhibitory Selaginella tamariscina extract and amentoflavone decrease the growth of A549 human lung cancer cells in vitro and in vivo.
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BACKGROUND
Selaginella tamariscina (P.Beauv.) Spring is a traditional medicinal plant used to treat various human diseases, including cancer, in Asia. The detailed molecular mechanism underlying the anti-cancer effects of this plant and the anti-cancer action of the combinatorial treatment of S.
Amentoflavone suppresses tumor growth in ovarian cancer by modulating Skp2.
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OBJECTIVE
Ovarian cancer is one of most common malignancies in women and is associated with high reoccurrence rate and poor prognosis. This study is designed to investigate the anti-tumor effects of amentoflavone (AF), one of the major active ingredients of S. tamariscina, against ovarian
Amentoflavone induces cell-cycle arrest and apoptosis in MCF-7 human breast cancer cells via mitochondria-dependent pathway.
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Amentoflavone, isolated from an ethyl acetate extract of the whole plant of Selaginella tamariscina, a traditional herb, may exhibit antitumor activity. The aim of this study was to investigate the anticancer mechanism(s) of amentoflavone, such as mitochondria-mediated apoptotic cell death, in
Amentoflavone Effectively Blocked the Tumor Progression of Glioblastoma via Suppression of ERK/NF- κ B Signaling Pathway.
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Glioblastoma is the most common primary malignant tumor of the central nervous system, with an annual incidence of 5.26 per 100000 people. The clinical outcome of standard therapy and the survival rate remain poor; therefore, there is an unmet need for a new strategy to treat this lethal disease.
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