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      Mechanistic Effects of Calcitriol in Cancer Biology

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          Abstract

          Besides its classical biological effects on calcium and phosphorus homeostasis, calcitriol, the active vitamin D metabolite, has a broad variety of actions including anticancer effects that are mediated either transcriptionally and/or via non-genomic pathways. In the context of cancer, calcitriol regulates the cell cycle, induces apoptosis, promotes cell differentiation and acts as anti-inflammatory factor within the tumor microenvironment. In this review, we address the different mechanisms of action involved in the antineoplastic effects of calcitriol.

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          NF-kappaB in cancer: from innocent bystander to major culprit.

          Michael Karin, Yixue Cao, Florian Greten … (2002)
          Nuclear factor of kappaB (NF-kappaB) is a sequence-specific transcription factor that is known to be involved in the inflammatory and innate immune responses. Although the importance of NF-KB in immunity is undisputed, recent evidence indicates that NF-kappaB and the signalling pathways that are involved in its activation are also important for tumour development. NF-kappaB should therefore receive as much attention from cancer researchers as it has already from immunologists.
          Article 0 comments Cited 542 times – based on 0 reviews     Review now
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            Stat3 as an oncogene.

            J. Bromberg, M Wrzeszczynska, G Devgan … (1999)
            STATs are latent transcription factors that mediate cytokine- and growth factor-directed transcription. In many human cancers and transformed cell lines, Stat3 is persistently activated, and in cell culture, active Stat3 is either required for transformation, enhances transformation, or blocks apoptosis. We report that substitution of two cysteine residues within the C-terminal loop of the SH2 domain of Stat3 produces a molecule that dimerizes spontaneously, binds to DNA, and activates transcription. The Stat3-C molecule in immortalized fibroblasts causes cellular transformation scored by colony formation in soft agar and tumor formation in nude mice. Thus, the activated Stat3 molecule by itself can mediate cellular transformation and the experiments focus attention on the importance of constitutive Stat3 activation in human tumors.
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              MYC inactivation uncovers pluripotent differentiation and tumour dormancy in hepatocellular cancer.

              Catherine M Shachaf, Andrew M. Kopelman, Constadina Arvanitis … (2004)
              Hepatocellular carcinoma is generally refractory to clinical treatment. Here, we report that inactivation of the MYC oncogene is sufficient to induce sustained regression of invasive liver cancers. MYC inactivation resulted en masse in tumour cells differentiating into hepatocytes and biliary cells forming bile duct structures, and this was associated with rapid loss of expression of the tumour marker alpha-fetoprotein, the increase in expression of liver cell markers cytokeratin 8 and carcinoembryonic antigen, and in some cells the liver stem cell marker cytokeratin 19. Using in vivo bioluminescence imaging we found that many of these tumour cells remained dormant as long as MYC remain inactivated; however, MYC reactivation immediately restored their neoplastic features. Using array comparative genomic hybridization we confirmed that these dormant liver cells and the restored tumour retained the identical molecular signature and hence were clonally derived from the tumour cells. Our results show how oncogene inactivation may reverse tumorigenesis in the most clinically difficult cancers. Oncogene inactivation uncovers the pluripotent capacity of tumours to differentiate into normal cellular lineages and tissue structures, while retaining their latent potential to become cancerous, and hence existing in a state of tumour dormancy.
              Article 0 comments Cited 259 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nutrients
                Journal ID (iso-abbrev): Nutrients
                Journal ID (publisher-id): nutrients
                Title: Nutrients
                Publisher: MDPI
                ISSN (Electronic): 2072-6643
                Publication date (Electronic): 19 June 2015
                Publication date Collection: June 2015
                Volume: 7
                Issue: 6
                Pages: 5020-5050
                Affiliations
                [1 ]Departamento de Biología de la Reproducción, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga No. 15, Tlalpan, Mexico City 14000, Mexico; E-Mail: lorenzadiaz@ 123456gmail.com
                [2 ]Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Campus UNAM-Juriquilla, Blvd. Juriquilla 3001, Querétaro 76230, Mexico; E-Mails: mdiaz@ 123456comunidad.unam.mx (M.D.-M.); acgarciag02@ 123456gmail.com (A.C.G.-G.)
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: isabelcm@ 123456unam.mx ; Tel./Fax: +52-442-238-1035.
                Article
                Publisher ID: nutrients-07-05020
                DOI: 10.3390/nu7065020
                PMC ID: 4488829
                PubMed ID: 26102214
                SO-VID: 9fd70133-e6e3-4100-91f7-3d9f2c149fcf
                Copyright © © 2015 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 03 May 2015
                Date accepted : 12 June 2015
                Categories
                Subject: Review

                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: calcitriol,cancer,inflammation,vitamin d deficiency,oncogenesis
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: calcitriol, cancer, inflammation, vitamin d deficiency, oncogenesis

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