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Journal of Environmental Pathology, Toxicology and Oncology

Published 4 issues per year

ISSN Print: 0731-8898

ISSN Online: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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13-cis-Retinoic Acid Induces Apoptosis by Modulating Caspase-3, bcl-2, and p53 Gene Expression and Regulates the Activation of Transcription Factors in B16F-10 Melanoma Cells

Volume 27, Issue 3, 2008, pp. 197-207
DOI: 10.1615/JEnvironPatholToxicolOncol.v27.i3.40
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ABSTRACT

Cancer prevention using natural products has become an integral part of cancer control. In this study we investigated the effect of 13-cis-retinoic acid on the induction of apoptosis as well as its regulatory effect on the activation of transcription factors in B16F-10 melanoma cells. Treatment of B16F-10 cells with 13-cis-retinoic acid showed the presence of apoptotic bodies and induced DNA fragmentation. 13-cis-retinoic acid treatment also showed an inhibitory effect on bcl-2 expression and upregulated p53 and caspase-3 gene expression in B16F-10 melanoma cells. The study also reveals that 13-cis-retinoic acid treatment could alter the production and expression of proinflammatory cytokines and could inhibit the activation and nuclear translocation of p65, p50, and c-Rel subunits of nuclear factor-nB, and other transcription factors such as c-fos, activated transcription factor-2, and cyclic adenosine monophosphate response element-binding protein in B16F-10 melanoma cells. These results suggest that 13-cis-retinoic acid effectively induces apoptosis in B16F-10 melanoma cells and this compound has the potential as either a therapeutic or chemotherapeutic agent against melanoma.

CITED BY
  1. Dhamne Sagar, Brown Robert E., Covinsky Michael, Dhamne Chetan, Eldin Karen, Tatevian Nina, Clear Cell Sarcoma of Kidney: Morphoproteomic Analysis Reveals Genomic Correlates and Therapeutic Options, Pediatric and Developmental Pathology, 16, 1, 2013. Crossref

  2. Silva Filomena S. G., Ribeiro Mariana P. C., Santos Maria S., Rocha-Pereira Petronila, Santos-Silva Alice, Custódio José B. A., The antiestrogen 4-hydroxytamoxifen protects against isotretinoin-induced permeability transition and bioenergetic dysfunction of liver mitochondria: comparison with tamoxifen, Journal of Bioenergetics and Biomembranes, 45, 4, 2013. Crossref

  3. Todaro Laura Beatriz, Veloso María José, Campodónico Paola Bernadette, Puricelli Lydia Inés, Farías Eduardo Francisco, Bal de Kier Joffé Elisa Dora, A clinically relevant bi-cellular murine mammary tumor model as a useful tool for evaluating the effect of retinoic acid signaling on tumor progression, Breast Cancer, 20, 4, 2013. Crossref

  4. Abali Remzi, Yuksel Mehmet Aytac, Aktas Cevat, Celik Cem, Guzel Savas, Erfan Gamze, Sahin Onder, Decreased ovarian reserve in female Sprague–Dawley rats induced by isotretinoin (retinoic acid) exposure, Reproductive BioMedicine Online, 27, 2, 2013. Crossref

  5. Silva F.S.G., Oliveira H., Moreiras A., Fernandes J.C., Bronze-da-Rocha E., Figueiredo A., Custódio J.B.A., Rocha-Pereira P., Santos-Silva A., The in vitro and in vivo genotoxicity of isotretinoin assessed by cytokinesis blocked micronucleus assay and comet assay, Toxicology in Vitro, 27, 2, 2013. Crossref

  6. Melnik Bodo, Isotretinoin and FoxO1, Dermato-Endocrinology, 3, 3, 2011. Crossref

  7. Griffin Jennifer N., Pinali Daniel, Olds Kaylan, Lu Na, Appleby Lindsay, Doan Louis, Lane Michelle A., 13-Cis-retinoic acid decreases hypothalamic cell number in vitro, Neuroscience Research, 68, 3, 2010. Crossref

  8. de Oliveira Marcos Roberto, Vitamin A and Retinoids as Mitochondrial Toxicants, Oxidative Medicine and Cellular Longevity, 2015, 2015. Crossref

  9. Drew C.J.G., O'Reilly K.C., Lane M.A., Bailey S.J., Chronic administration of 13-cis-retinoic acid does not alter the number of serotoninergic neurons in the mouse raphe nuclei, Neuroscience, 172, 2011. Crossref

  10. Muñiz-Hernández Saé, Hernández-Pedro Norma, Macedo-Pérez Omar E., Arrieta Oscar, Alterations in Retinoic Acid Receptors in Non-Small Cell Lung Cancer and Their Clinical Implications, Journal of Cancer Therapy, 06, 08, 2015. Crossref

  11. Melnik Bodo C., p53: key conductor of all anti-acne therapies, Journal of Translational Medicine, 15, 1, 2017. Crossref

  12. Amann Philipp M., Czaja Katharina, Bazhin Alexandr V., Rühl Ralph, Eichmüller Stefan B., Merk Hans F., Baron Jens M., LRAT Overexpression Diminishes Intracellular Levels of Biologically Active Retinoids and Reduces Retinoid Antitumor Efficacy in the Murine Melanoma B16F10 Cell Line, Skin Pharmacology and Physiology, 28, 4, 2015. Crossref

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