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      Leukemia Inhibitory Factor Downregulates Human Papillomavirus-16 Oncogene Expression and Inhibits the Proliferation of Cervical Carcinoma Cells

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          Abstract

          The constitutive proliferation and resistance to differentiation and apoptosis of neoplastic cervical cells depend on sustained expression of human papillomavirus oncogenes. Inhibition of these oncogenes is a goal for the prevention of progression of HPV-induced neoplasias to cervical cancer. SiHa cervical cancer cells were transfected with an HPV-16 promoter reporter construct and treated with leukemia inhibitory factor (LIF), a human cytokine of the interleukin 6 superfamily. SiHa and CaSki cervical cancer cells were also assessed for proliferation by MTT precipitation, programmed cell death by flow cytometry, and HPV E6 and E7 expression by real-time PCR. LIF-treated cervical cancer cells showed significantly reduced HPV LCR activation, reduced levels of E6 and E7 mRNA, and reduced proliferation. We report the novel use of LIF to inhibit viral oncogene expression in cervical cancer cells, with concomitant reduction in proliferation suggesting re-engagement of cell-cycle regulation.

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          Papillomaviruses causing cancer: evasion from host-cell control in early events in carcinogenesis.

          H zur Hausen (2000)
          During the past 20 years, several types of human papillomaviruses (HPVs) have been identified that cause specific types of cancers. The etiology of cancer of the cervix has been linked to several types of HPV, with a high preponderance of HPV16. The role of these virus infections has been established 1) by the regular presence of HPV DNA in the respective tumor biopsy specimens, 2) by the demonstration of viral oncogene expression (E6 and E7) in tumor material, 3) by the identification of transforming properties of these genes, 4) by the requirement for E6 and E7 expression for maintaining the malignant phenotype of cervical carcinoma cell lines, 5) by the interaction of viral oncoproteins with growth-regulating host-cell proteins, and 6) by epidemiologic studies pointing to these HPV infections as the major risk factor for cervical cancer development. In addition to cancer of the cervix, a major proportion of anal, perianal, vulvar, and penile cancers appears to be linked to the same HPV infections. In addition, close to 20% of oropharyngeal cancers contain DNA from the same types of HPV. Recent evidence also points to a possible role of other HPV infections in squamous cell carcinomas of the skin. This review covers recent developments in understanding molecular mechanisms of HPV carcinogenesis, mainly discussing functions of viral oncoproteins and the regulation of viral oncogenes by host-cell factors. Modifications in host-cell genes, most likely engaged in the control of HPV gene expression in proliferating cells, emerge as important events in HPV-mediated carcinogenesis.
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            Association and activation of Jak-Tyk kinases by CNTF-LIF-OSM-IL-6 beta receptor components.

            Pietro G Barbieri, S Boulton, N Ståhl … (1994)
            A recently defined family of cytokines, consisting of ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF), oncostatin M (OSM), and interleukin-6 (IL-6), utilize the Jak-Tyk family of cytoplasmic tyrosine kinases. The beta receptor components for this cytokine family, gp130 and LIF receptor beta, constitutively associate with Jak-Tyk kinases. Activation of these kinases occurs as a result of ligand-induced dimerization of the receptor beta components. Unlike other cytokine receptors studied to date, the receptors for the CNTF cytokine family utilize all known members of the Jak-Tyk family, but induce distinct patterns of Jak-Tyk phosphorylation in different cell lines.
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              Human papillomaviruses in the pathogenesis of anogenital cancer.

              H zur Hausen (1991)
              Substantial experimental evidence accumulated over the past 8 years has indicated an etiological role for specific human papillomavirus (HPV) types in anogenital cancer and its premalignant precursors. Virus infection and viral gene expression emerge as necessary but obviously not sufficient factors for cancer induction. Additional modifications of host cell genes appear to be required for malignant progression of infected cells. The expression of viral oncoproteins in cells infected by "high-risk" types (e.g., HPV 16, HPV 18), in contrast to "low-risk" types (e.g., HPV 6, HPV 11), results in chromosomal instability and apparently in accumulation of mutational events. These "endogenous" modifications seem to be most important in the pathogenesis of premalignant lesions and tumor progression. Exogenous mutagens should act as additional cofactors.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Infect Dis Obstet Gynecol
                Journal ID (publisher-id): IDOG
                Title: Infectious Diseases in Obstetrics and Gynecology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1064-7449
                ISSN (Electronic): 1098-0997
                Publication date (Print): 2011
                Publication date (Electronic): 4 June 2011
                Volume: 2011
                Electronic Location Identifier: 463081
                Affiliations
                1Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford CA 94305-5317, USA
                2Department of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford CA 94305-5317, USA
                Author notes
                *Nelson N. H. Teng: teng@ 123456stanford.edu

                Academic Editor: Ann Duerr

                Article
                DOI: 10.1155/2011/463081
                PMC ID: 3124004
                PubMed ID: 21747640
                SO-VID: fc18ad91-e3d7-4bef-a1af-e503f56ea3b3
                Copyright © Copyright © 2011 Joseph M. Bay et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 2 December 2010
                Date accepted : 7 April 2011
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Obstetrics & Gynecology
                Data availability:
                ScienceOpen disciplines: Obstetrics & Gynecology

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