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    Millipore cuminaldehyde
    Inhibition of NCI-H520 topoisomerase I and II activities by CuA. (A) CuA inhibited topoisomerase I activity in NCI-H520 cells. Nuclear proteins from NCI-H520 cells were added to a specific topoisomerase I reaction mixture in the presence of the indicated concentrations of CuA (lanes 3-5), or 60 μM CPT (lane 6), or the vehicle (1% DMSO, lane 2). Lane 1: pUC19 DNA only. (B) CuA inhibits topoisomerase II activity in NCI-H520 cells. DNA relaxation assay (upper part) and decatenation assay (lower part): Nuclear proteins from NCI-H520 cells were added to a specific topoisomerase II reaction mixture in the presence of the indicated concentrations of CuA (lanes 3-5) or 60 μM VP-16, a specific topoisomerase II inhibitor (lane 6), or the vehicle (1% DMSO, lane 2). (Lane 1) Supercoiled pUC19 DNA (upper part) or kDNA (lower part) only. kDNA is a large network of plasmids, and when it is analyzed by gel electrophoresis, it penetrates only slightly into agarose gel (result not shown). Upon decatenation by topoisomerase II, mini circles monomers of kDNA were formed (lower part, lanes 2-6). CPT, camptothecin; CuA, <t>cuminaldehyde;</t> S and R, supercoiled and the relaxed forms of the pUC 19 plasmid DNA, respectively; VP-16, etoposide.
    Cuminaldehyde, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Inhibition of NCI-H520 topoisomerase I and II activities by CuA. (A) CuA inhibited topoisomerase I activity in NCI-H520 cells. Nuclear proteins from NCI-H520 cells were added to a specific topoisomerase I reaction mixture in the presence of the indicated concentrations of CuA (lanes 3-5), or 60 μM CPT (lane 6), or the vehicle (1% DMSO, lane 2). Lane 1: pUC19 DNA only. (B) CuA inhibits topoisomerase II activity in NCI-H520 cells. DNA relaxation assay (upper part) and decatenation assay (lower part): Nuclear proteins from NCI-H520 cells were added to a specific topoisomerase II reaction mixture in the presence of the indicated concentrations of CuA (lanes 3-5) or 60 μM VP-16, a specific topoisomerase II inhibitor (lane 6), or the vehicle (1% DMSO, lane 2). (Lane 1) Supercoiled pUC19 DNA (upper part) or kDNA (lower part) only. kDNA is a large network of plasmids, and when it is analyzed by gel electrophoresis, it penetrates only slightly into agarose gel (result not shown). Upon decatenation by topoisomerase II, mini circles monomers of kDNA were formed (lower part, lanes 2-6). CPT, camptothecin; CuA, cuminaldehyde; S and R, supercoiled and the relaxed forms of the pUC 19 plasmid DNA, respectively; VP-16, etoposide.

    Journal: Journal of Cancer

    Article Title: Molecular Mechanism of Cinnamomum verum Component Cuminaldehyde Inhibits Cell Growth and Induces Cell Death in Human Lung Squamous Cell Carcinoma NCI-H520 Cells In Vitro and In Vivo

    doi: 10.7150/jca.13689

    Figure Lengend Snippet: Inhibition of NCI-H520 topoisomerase I and II activities by CuA. (A) CuA inhibited topoisomerase I activity in NCI-H520 cells. Nuclear proteins from NCI-H520 cells were added to a specific topoisomerase I reaction mixture in the presence of the indicated concentrations of CuA (lanes 3-5), or 60 μM CPT (lane 6), or the vehicle (1% DMSO, lane 2). Lane 1: pUC19 DNA only. (B) CuA inhibits topoisomerase II activity in NCI-H520 cells. DNA relaxation assay (upper part) and decatenation assay (lower part): Nuclear proteins from NCI-H520 cells were added to a specific topoisomerase II reaction mixture in the presence of the indicated concentrations of CuA (lanes 3-5) or 60 μM VP-16, a specific topoisomerase II inhibitor (lane 6), or the vehicle (1% DMSO, lane 2). (Lane 1) Supercoiled pUC19 DNA (upper part) or kDNA (lower part) only. kDNA is a large network of plasmids, and when it is analyzed by gel electrophoresis, it penetrates only slightly into agarose gel (result not shown). Upon decatenation by topoisomerase II, mini circles monomers of kDNA were formed (lower part, lanes 2-6). CPT, camptothecin; CuA, cuminaldehyde; S and R, supercoiled and the relaxed forms of the pUC 19 plasmid DNA, respectively; VP-16, etoposide.

    Article Snippet: Cuminaldehyde (CuA) and dimethyl sulfoxide (DMSO) were purchased from Sigma-Aldrich, Inc. (St. Louis, Mo, USA).

    Techniques: Inhibition, Activity Assay, Cycling Probe Technology, Nucleic Acid Electrophoresis, Agarose Gel Electrophoresis, Plasmid Preparation

    Cuminaldehyde induced apoptosis through the mitochondrial pathway in NCI-H520 cells. (A and B) Cells were treated with the indicated concentrations of cuminaldehyde for 48 h. Levels of Bax, Bak, Bcl-2, Bcl-XL, and cytochrome c were evaluated by Western blotting using specific antibodies; the cytoplasm and mitochondria fractions were extracted from cell pellets. (A) Expressions of Bcl-2 family proteins. (B) Release of cytochrome c from mitochondria into cytosol. (C) Cuminaldehyde induced mitochondrial depolarization. (C, left) Cells were treated with the indicated concentrations of cuminaldehyde for 24 h and ΔΨ m was analyzed by JC-1 using fluorescence microscopy: (Left, upper part) Control cells with intact mitochondria fluorescencing red; (Left, lower part) Most cuminaldehyde-treated cells fluorescencing green, suggesting the loss of ΔΨ m ; (Right part) Cells were treated with the indicated concentrations of cuminaldehyde for 24 h and ΔΨ m was analyzed by JC-1 using spectrophotometer. (D) Activations of caspase-3 and -9. Cells were treated with the indicated concentrations of cuminaldehyde for 24 h and activities of caspases-3 and -9 were determined fluorometrically using fluorescence-labeled synthetic substrates. Data are expressed as means ± standard error of mean, n = 3. *Indicates a significant difference ( p

    Journal: Journal of Cancer

    Article Title: Molecular Mechanism of Cinnamomum verum Component Cuminaldehyde Inhibits Cell Growth and Induces Cell Death in Human Lung Squamous Cell Carcinoma NCI-H520 Cells In Vitro and In Vivo

    doi: 10.7150/jca.13689

    Figure Lengend Snippet: Cuminaldehyde induced apoptosis through the mitochondrial pathway in NCI-H520 cells. (A and B) Cells were treated with the indicated concentrations of cuminaldehyde for 48 h. Levels of Bax, Bak, Bcl-2, Bcl-XL, and cytochrome c were evaluated by Western blotting using specific antibodies; the cytoplasm and mitochondria fractions were extracted from cell pellets. (A) Expressions of Bcl-2 family proteins. (B) Release of cytochrome c from mitochondria into cytosol. (C) Cuminaldehyde induced mitochondrial depolarization. (C, left) Cells were treated with the indicated concentrations of cuminaldehyde for 24 h and ΔΨ m was analyzed by JC-1 using fluorescence microscopy: (Left, upper part) Control cells with intact mitochondria fluorescencing red; (Left, lower part) Most cuminaldehyde-treated cells fluorescencing green, suggesting the loss of ΔΨ m ; (Right part) Cells were treated with the indicated concentrations of cuminaldehyde for 24 h and ΔΨ m was analyzed by JC-1 using spectrophotometer. (D) Activations of caspase-3 and -9. Cells were treated with the indicated concentrations of cuminaldehyde for 24 h and activities of caspases-3 and -9 were determined fluorometrically using fluorescence-labeled synthetic substrates. Data are expressed as means ± standard error of mean, n = 3. *Indicates a significant difference ( p

    Article Snippet: Cuminaldehyde (CuA) and dimethyl sulfoxide (DMSO) were purchased from Sigma-Aldrich, Inc. (St. Louis, Mo, USA).

    Techniques: Western Blot, Fluorescence, Microscopy, Spectrophotometry, Labeling

    CuA suppressed growth and induced apoptosis in NCI-H520 xenograft. Animals bearing pre-established tumors ( n = 6 per group) were injected intratumorally with CuA (10 mg/kg/day) or vehicle. During the 50-day CuA treatment, tumor volumes were monitored using calipers and apoptosis was assessed by TUNEL assay. (A) Left: Representative tumor-possessing nude mice from the control (upper part) and CuA-treated (lower part) groups. (A) Right: CuA induced apoptosis in NCI-H520 xenograft by TUNEL assay. Representative TUNEL assays of tumors from the control (upper part) and CuA-treated (lower part) groups. (B) Means of tumor volume measured at the indicated number of days after implantation. CuA, cuminaldehyde.

    Journal: Journal of Cancer

    Article Title: Molecular Mechanism of Cinnamomum verum Component Cuminaldehyde Inhibits Cell Growth and Induces Cell Death in Human Lung Squamous Cell Carcinoma NCI-H520 Cells In Vitro and In Vivo

    doi: 10.7150/jca.13689

    Figure Lengend Snippet: CuA suppressed growth and induced apoptosis in NCI-H520 xenograft. Animals bearing pre-established tumors ( n = 6 per group) were injected intratumorally with CuA (10 mg/kg/day) or vehicle. During the 50-day CuA treatment, tumor volumes were monitored using calipers and apoptosis was assessed by TUNEL assay. (A) Left: Representative tumor-possessing nude mice from the control (upper part) and CuA-treated (lower part) groups. (A) Right: CuA induced apoptosis in NCI-H520 xenograft by TUNEL assay. Representative TUNEL assays of tumors from the control (upper part) and CuA-treated (lower part) groups. (B) Means of tumor volume measured at the indicated number of days after implantation. CuA, cuminaldehyde.

    Article Snippet: Cuminaldehyde (CuA) and dimethyl sulfoxide (DMSO) were purchased from Sigma-Aldrich, Inc. (St. Louis, Mo, USA).

    Techniques: Injection, TUNEL Assay, Mouse Assay