Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P42574 (caspase-3)
 45,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

N-butylidenephthalide (BP), isolated from the chloroform extract of Angelica sinensis, has been examined for its antitumor effects on glioblastoma multiforme brain tumors; however, little is known about its antitumor effects on hepatocellular carcinoma cells. Two hepatocellular carcinoma cell lines, HepG2 and J5, were treated with either N-butylidenephthalide or a vehicle, and cell viability and apoptosis were evaluated. Apoptosis-related mRNA and proteins expressed, including orphan receptor family Nurr1, NOR-1, and Nur77, were evaluated as well as the effect of N-butylidenephthalide in an in vivo xenograft model. N-butylidenephthalide caused growth inhibition of both the cell lines at 25 microg/ml. Furthermore, N-butylidenephthalide-induced apoptosis seems to be related to Nur77 translocation from nucleus to cytosol, which leads to cytochrome c release and caspase-3-dependent apoptosis. N-butylidenephthalide-related tumor apoptosis was associated with phosphatidylinositol 3-kinase/protein kinase B (AKT)/glycogen synthase kinase-3beta rather than the mitogen-activated protein kinase or protein kinase C pathway. Blockade of AKT activation enhanced proliferation inhibition and the induction of phosphor-Bcl-2 and Nur77 proteins. Besides, the increasing apoptosis by BP via transfection wild-type cAMP-response element-binding protein (CREB) into tumor cell was suppressed by dominant phosphorylation site mutation of CREB. This finding suggested CREB pathway was also partly involved in tumor apoptosis caused by BP. Administration of N-butylidenephthalide showed similar antitumoral effects in both HepG2 and J5 xenograft tumors. N-Butylidenephthalide induced apoptosis in hepatocellular carcinoma cells, both in vitro and in vivo, suggesting a potential clinical use of this compound for improving the prognosis of hepatocellular carcinoma cells.
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PMID:The induction of orphan nuclear receptor Nur77 expression by n-butylenephthalide as pharmaceuticals on hepatocellular carcinoma cell therapy. 1857 87

n-Butylidenephthalide (BP) is a potential anti-cancer drug, which can be extracted from Angelica sinensis (Danggui). Previous reports have shown the effectiveness of BP in treating cancer diseases. However, BP has no targeting capacity towards specific cancer cells. To improve treatment efficiency and reduce the dose of BP used in cancer treatment, targeting-based approaches should be developed. In the present study, we used riboflavin-5'-phosphate (RFMP) immobilized iron oxide magnetic nanoparticles (Fe3O4 MNPs) as carriers for BP to treat cancer cell lines derived from liver, prostate and breast. These model cancer cells overexpress riboflavin receptors on their cell membrane and are also sensitive to BP treatment. Thus, BP-binding free RFMP on MNPs can be used as probes to target these model cells, whereas BP can be readily released on target cancer cells. Cell viability was twofold lower by using Fe3O4@RFMP MNPs immobilized with BP than that achieved by using free-form BP at a similar amount. Moreover, BP-Fe3O4@RFMP MNPs have no apparent harmful effects on non-target cells. In addition, we evaluated the level of cysteine-aspartic acid protease 3 (caspase 3) in the resultant cell lysate obtained after treatment by BP-Fe3O4@RFMP MNPs to demonstrate that apoptosis is mainly involved in the growth inhibition of target cells.
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PMID:Riboflavin immobilized Fe3O4 magnetic nanoparticles carried with n-butylidenephthalide as targeting-based anticancer agents. 3066 4