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Apoptosis Induction

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Min Gu – 1st expert on this subject based on the ideXlab platform

  • Surface plasmonic gold nanorods for enhanced two-photon microscopic imaging and Apoptosis Induction of cancer cells.
    Biomaterials, 2010
    Co-Authors: Jing Liang Li, Min Gu

    Abstract:

    Two-photon microscopy powered by a femtosecond laser is a promising tool for luminescence imaging and localized microsurgery of cancers. However, the high energy required to destruct cells limits its medical applications. In this work, gold nanorods were conjugated with transferrin for efficient targeting, two-photon luminescence imaging and enhanced microsurgery of cancer cells. Due to the large two-photon excitation cross section of gold nanorods, gold nanorods are a hundred times more efficient than Fluorescein isothiocyanate (FITC), a common molecular dye, in three-dimensional imaging of cancer cells. The enhanced light absorption and energy conversion by gold nanorods enable treatment of cells with energy fluences two orders of magnitude below that in the absence of gold nanorods. By manipulating the energy fluence, Apoptosis of cancer cells has been achieved. At a same power density, the energy fluence for Apoptosis Induction is less than 20% of that for necrosis. Gold nanorods-enhanced luminescence imaging coupled with Apoptosis Induction of cancer cells provides a medically safe femtosecond laser-based imaging and microsurgery system for cancer diagnosis and treatment.

  • Surface plasmonic gold nanorods for enhanced two-photon microscopic imaging and Apoptosis Induction of cancer cells
    Biomaterials, 2010
    Co-Authors: Jing Liang Li, Min Gu

    Abstract:

    Two-photon microscopy powered by a femtosecond laser is a promising tool for luminescence imaging and localized microsurgery of cancers. However, the high energy required to destruct cells limits its medical applications. In this work, gold nanorods were conjugated with transferrin for efficient targeting, two-photon luminescence imaging and enhanced microsurgery of cancer cells. Due to the large two-photon excitation cross section of gold nanorods, gold nanorods are a hundred times more efficient than Fluorescein isothiocyanate (FITC), a common molecular dye, in three-dimensional imaging of cancer cells. The enhanced light absorption and energy conversion by gold nanorods enable treatment of cells with energy fluences two orders of magnitude below that in the absence of gold nanorods. By manipulating the energy fluence, Apoptosis of cancer cells has been achieved. At a same power density, the energy fluence for Apoptosis Induction is less than 20% of that for necrosis. Gold nanorods-enhanced luminescence imaging coupled with Apoptosis Induction of cancer cells provides a medically safe femtosecond laser-based imaging and microsurgery system for cancer diagnosis and treatment. © 2010 Elsevier Ltd.

Ramida Watanapokasin – 2nd expert on this subject based on the ideXlab platform

  • Antiproliferation and Apoptosis Induction in Colorectal Cancer Cells by Goniothalamin.
    Journal of the Medical Association of Thailand = Chotmaihet thangphaet, 2020
    Co-Authors: Thanet Sophonnithiprasert, Wilawan Mahabusarakam, Yukio Nakamura, Ramida Watanapokasin

    Abstract:

    To investigate the effect of goniothalamin on antiproliferation and Apoptosis Induction in three types of colorectal cancer cells.
    Colorectal cancer is the third of the twentieth most commonly diagnosed cancer. Different types of colorectal cancer cells differ in genotype and characteristics leading to different responses to anticancer drugs. Therefore, finding new anticancer compound for the colorectal cancer cells is necessary.
    Antiproliferative response of goniothalamin on three colorectal cancer cell lines including Colo 205, SW480, and LoVo were determined by MTT assay. The antiproliferative response at different time and dose was also observed. Apoptosis Induction by goniothalamin was observed in all three cell-lines via morphological changes and nuclear condensation by Hoechst33342 staining.
    Goniothalamin showed different antiproliferative response on Colo 205, SW480, and Lo Vo cells at the IC50 value is 9.86 ± 0.38 µM, 22.00 ± 4.40 µM, and 65.25 ± 1.85 µM respectively. In addition, the antiproliferative response of goniothalamin was a time- and dose-dependent manner Apoptosis morphological changes and nuclear condensation were clearly observed in Colo 205, SW480 and LoVo cells treated with 10 µM, 25 µM, and 50 µM goniothalamin, respectively.
    Goniothalamin showed antiproliferation and Apoptosis Induction in colorectal cancer cells with different sensitivity depending on cell type. Investigation of mechanisms underlying Apoptosis and its potential use for colorectal cancer treatment should be further studied.

  • Anti-Proliferation and Apoptosis Induction in Breast Cancer Cells by Cratoxylum cochinchinense Extract.
    Journal of the Medical Association of Thailand = Chotmaihet thangphaet, 2020
    Co-Authors: Sukanda Innajak, Wilawan Mahabusarakam, Sirinun Nilwarangoon, Ramida Watanapokasin

    Abstract:

    Breast cancer is the most common invasive cancer in females worldwide. It was found about 37.5% in Thai
    females and is one of the leading causes of death-related cancers in women. Therefore, new finding of anti-cancer compound as a therapeutic candidate in breast cancer is necessary.
    To investigate the effect of Cratoxylum cochinchinense extract on anti-proliferation and Apoptosis Induction in breast cancer cells.
    Cell proliferation and cell viability assay were determined by MTT assay. Hoechst 33342 and JC-1 staining were used to determined nuclear morphological changes and mitochondrial membrane potential, respectively.
    C. cochinchinense extract showed anti-proliferation in MDA-MB-468 treated cells in a time- and dose-dependent manner with IC50 value of 19.19+0.8 μg/ml. In addition, C. cochinchinense extract induced nuclear condensation and apoptotic bodies in MDA-MB-468 treated cells. JC-1 staining revealed that C. cochinchinense extract induced mitochondrial membrane dysfunction.
    C. cochinchinense extract showed anti-proliferation and Apoptosis Induction properties in MDA-MB-468
    treated cells. These results suggested that C. cochinchinense extract may be a potential candidate for anti-cancer drug developing. The underlying mechanisms of Apoptosis Induction should be further studied.

  • Mechanism of Apoptosis Induction associated with ERK1/2 upregulation via goniothalamin in melanoma cells
    Experimental and Therapeutic Medicine, 2018
    Co-Authors: Suphakorn Tangchirakhaphan, Sukanda Innajak, Sirinun Nilwarangkoon, Nudjaree Tanjapatkul, Wilawan Mahabusrakum, Ramida Watanapokasin

    Abstract:

    The present study aimed to investigate the effect of goniothalamin on Apoptosis Induction in the A375 melanoma cell line. Melanoma is a type of skin cancer with increased prevalence and no potential standard treatment. Goniothalamin is a plant, bioactive styrly-lactone, which has various bioactivities including anti-microbial, anti-inflammatory and anti-cancer. Apoptosis Induction by goniothalamin has been studied in numerous cancer cell lines, however not in the melanoma cell line A375. The results of the MTT assay demonstrated that goniothalamin induced anti-proliferation in a dose dependent manner. Hoechst staining assay demonstrated that goniothalamin induced chromatin condensation and apoptotic bodies in A375 treated cells, and JC-1 staining revealed that goniothalamin induced mitochondrial membrane dysfunction in A375 cells. In addition, goniothalamin decreased the level of anti-apoptotic proteins myeloid cell leukemia 1, B cell lymphoma (Bcl)-2 and Bcl-extra large, whereas it increased the level of pro-apoptotic proteins, Bcl-2 Associated X, Apoptosis regulator, t-BID and Bim in A375 treated cells. In addition, goniothalamin also increased active caspase-9, -7 and cleaved-poly (ADP-ribose) polymerase expression in A375 treated cells. Furthermore, phosphorylated (p)-pyruvate dehydrogenase kinase (PDK) 1 (Ser241) and p-RAC-alpha serine/threonine-protein kinase (Akt; Ser473) were decreased, however c-Jun and p-extracellular signal-regulated kinase (ERK)1/2 were increased upon goniothalamin treatment. These results suggest that goniothalamin has an effect, as anti-proliferation and Apoptosis Induction in A375 cells were associated with upregulated p-ERK1/2, c-Jun and downregulated p-PDK1 (Ser241), p-Akt (Ser473) in A375 cells. Therefore, goniothalamin may be a potential candidate for anti-cancer drug development for melanoma treatment.

Georg Bauer – 3rd expert on this subject based on the ideXlab platform

  • Nitric oxide mediates Apoptosis Induction selectively in transformed fibroblasts compared to nontransformed fibroblasts
    Carcinogenesis, 2020
    Co-Authors: Stefanie Heigold, Christine Sers, Wibke Bechtel, Boris Ivanovas, Reinhold Schäfer, Georg Bauer

    Abstract:

    Nitric oxide (NO) mediates Apoptosis Induction in fibroblasts with constitutive src or induced ras oncogene expression, whereas nontransformed parental cells and revertants are not affected. This direct link between the transformed phenotype and sensitivity to NO-mediated Apoptosis Induction seems to be based on the recently described extracellular superoxide anion generation by transformed cells, as NO-mediated Apoptosis Induction in transformed cells is inhibited by extracellular superoxide dismutase (SOD), by SOD mimetics and by apocynin, an inhibitor of NADPH oxidase. Furthermore, nonresponsive nontransformed cells can be rendered sensitive for NOmediated Apoptosis Induction when they are supplemented with xanthine oxidase/xanthine as an extracellular source for superoxide anions. As superoxide anions and NO readily interact in a diffusion-controlled reaction to generate peroxynitrite, peroxynitrite seems to be the responsible Apoptosis inducer in NO-mediated Apoptosis Induction. In line with this conclusion, NO-mediated Apoptosis Induction in superoxide anion-generating transformed cells is inhibited by the peroxynitrite scavengers ebselen and FeTPPS. Moreover, direct application of peroxynitrite induces Apoptosis both in transformed and nontransformed cells, indicating that peroxynitrite is no selective Apoptosis inducer per se, but that selective Apoptosis Induction in transformed cells by NO is achieved through selective peroxynitrite generation. The interaction of NO with target cell derived superoxide anions represents a novel concept for selective Apoptosis Induction in transformed cells. This mechanism may be the basis for selective Apoptosis Induction by natural antitumor systems (like macrophages, natural killer cells, granulocytes) that utilize NO for antitumor action. Apoptosis Induction mediated by NO involves mitochondrial depolarization and is blocked by Bcl-2 overexpression.

  • Transformed target cell-derived superoxide anions drive Apoptosis Induction by myeloperoxidase.
    Redox Report, 2020
    Co-Authors: I. Engelmann, S. Dormann, M. Saran, Georg Bauer

    Abstract:

    Abstract Myeloperoxidase induces Apoptosis in src- or ras-transformed fibroblasts, but not in parental non-transformed fibroblasts. This selectivity seems to be based on superoxide anion production by transformed cells, a recently described characteristic feature of transformed cells. Myeloperoxidase-mediated Apoptosis Induction is inhibited by SOD, catalase, 4-aminobenzoyl hydrazide, taurine and DMSO. This pattern of inhibition allows us to conclude that transformed cell derived superoxide anions dismutate to hydrogen peroxide, which fosters HOCl formation by myeloperoxidase. Hydrogen peroxide formation thereby is the rate-limiting step and depends on the cell density. In a second step, HOCl interacts with superoxide anions to yield the highly reactive Apoptosis inducing hydroxyl radical. This conclusion was verified through selective Apoptosis Induction in transformed cells by direct addition of HOCl, which was also inhibited by SOD and DMSO. Our findings demonstrate a specific interplay between target …

  • Differential Role of Extra- and Intracellular Superoxide Anions for Nitric Oxide-mediated Apoptosis Induction
    in Vivo, 2004
    Co-Authors: Mareike Steinmann, Nicolas Moosmann, Mareike Schimmel, Christina Gerhardus, Georg Bauer

    Abstract:

    Nitric oxide (NO) has recently been shown to mediate Apoptosis Induction selectively in transformed fibroblasts, in contrast to their nontransformed parental cells. Here we show that NO-mediated Apoptosis Induction in transformed fibroblasts can be divided into two major phases. During phase 1, peroxynitrite is generated by the interaction of extracellular superoxide anions with NO and the intracellular glutathione level is subsequently lowered. This defines the beginning of phase 2, in which NO-mediated signaling depends on intracellular superoxide anions exclusively. The resultant peroxynitrite seems to activate the mitochondrial permeability transition pore and thus triggers execution of Apoptosis. Experimental depletion of intracellular glutathione causes a drastic decrease in the length of phase 1 in transformed cells and renders nontransformed cells sensitive to NO-mediated Apoptosis Induction. These findings allow the prediction that either Induction of superoxide anion generation or glutathione depletion may render cells sensitive to NO-mediated Apoptosis Induction. Nitric oxide (NO) is a free radical with diverse biological functions of central importance (1, for review see ref. 2). It arises from the guanodino group of L-arginine in a NADPH- dependent reaction catalyzed by constitutively expressed or inducible NO synthases (NOS). NO is able to pass cellular membranes (3), to decrease the intracellular glutathione pool (4), to regulate gene expression via interaction with the zinc finger transcription factor SP1 (5) and to up-regulate p53 gene expression (6). The neurotrophic function of NO switches to cell death Induction in midbrain cultures after glutathione depletion (7). Direct Apoptosis Induction by NO has been reported for