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      Induction of BCL2-Interacting Killer, BIK, is Mediated for Anti-Cancer Activity of Curcumin in Human Head and Neck Squamous Cell Carcinoma Cells

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          Abstract

          Naturally occurring diarylheptanoid curcumin (CUR), a principal component of the Asian spice turmeric, has been shown to have anti-cancer effects in many tumor types. However, a detailed mechanism regarding CUR induced tumor cell killing remain to be comprehensively explored. Using two head neck squamous cell carcinoma (HNSCC) cell lines FaDu (hypopharyngeal) and Cal27 (tongue), we demonstrated a novel mechanism by which CUR levies the cytotoxic effect. We found that CUR induced upregulation of pro-apoptotic Bik, down-regulation of survival signaling by AKT and NF-κB prior to the induction of the caspase-cascade reduction of cell proliferation, are primary mechanisms of CUR-induced cell death, thus providing insights into the anti-tumor activity of CUR in HNSCC cells.

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          Most cited references43

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          Cell death: critical control points.

          Nika Danial, Stanley Korsmeyer (2004)
          Programmed cell death is a distinct genetic and biochemical pathway essential to metazoans. An intact death pathway is required for successful embryonic development and the maintenance of normal tissue homeostasis. Apoptosis has proven to be tightly interwoven with other essential cell pathways. The identification of critical control points in the cell death pathway has yielded fundamental insights for basic biology, as well as provided rational targets for new therapeutics.
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            Cancer statistics, 2007.

            Ahmedin Jemal, Rebecca Siegel, Elizabeth Ward … (2007)
            Each year, the American Cancer Society (ACS) estimates the number of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute, Centers for Disease Control and Prevention, and the North American Association of Central Cancer Registries and mortality data from the National Center for Health Statistics. This report considers incidence data through 2003 and mortality data through 2004. Incidence and death rates are age-standardized to the 2000 US standard million population. A total of 1,444,920 new cancer cases and 559,650 deaths for cancers are projected to occur in the United States in 2007. Notable trends in cancer incidence and mortality rates include stabilization of the age-standardized, delay-adjusted incidence rates for all cancers combined in men from 1995 through 2003; a continuing increase in the incidence rate by 0.3% per year in women; and a 13.6% total decrease in age-standardized cancer death rates among men and women combined between 1991 and 2004. This report also examines cancer incidence, mortality, and survival by site, sex, race/ethnicity, geographic area, and calendar year, as well as the proportionate contribution of selected sites to the overall trends. While the absolute number of cancer deaths decreased for the second consecutive year in the United States (by more than 3,000 from 2003 to 2004) and much progress has been made in reducing mortality rates and improving survival, cancer still accounts for more deaths than heart disease in persons under age 85 years. Further progress can be accelerated by supporting new discoveries and by applying existing cancer control knowledge across all segments of the population.
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              An essential role for NF-kappaB in preventing TNF-alpha-induced cell death.

              A Beg, D Baltimore (1996)
              Studies on mice deficient in nuclear factor kappa B (NF-kappaB) subunits have shown that this transcription factor is important for lymphocyte responses to antigens and cytokine-inducible gene expression. In particular, the RelA (p65) subunit is required for induction of tumor necrosis factor-alpha (TNF-alpha)-dependent genes. Treatment of RelA-deficient (RelA-/-) mouse fibroblasts and macrophages with TNF-alpha resulted in a significant reduction in viability, whereas RelA+/+ cells were unaffected. Cytotoxicity to both cell types was mediated by TNF receptor 1. Reintroduction of RelA into RelA-/- fibroblasts resulted in enhanced survival, demonstrating that the presence of RelA is required for protection from TNF-alpha. These results have implications for the treatment of inflammatory and proliferative diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cancer
                Journal ID (iso-abbrev): J Cancer
                Journal ID (publisher-id): jca
                Title: Journal of Cancer
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1837-9664
                Publication date Collection: 2015
                Publication date (Electronic): 12 February 2015
                Volume: 6
                Issue: 4
                Pages: 327-332
                Affiliations
                1. The Key Laboratory of Pathobiology, Ministry of Education, Norman Bethune College of Medicine, Jilin University, Changchun 130021, China
                2. Carmen and Ann Adams Department of Pediatrics, Department of Otolaryngology, Wayne State University, Detroit, MI 48201, USA
                3. Molecular Therapeutics Program, Karmanos Cancer Institute, Detroit, MI 48201, USA
                4. Division of Hematology/Oncology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, 35294, USA
                Author notes
                ✉ Corresponding authors: Qinghua Zeng: zengnwu@ 123456yahoo.com or Yu-lin Li: ylli@ 123456jlu.edu.cn

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                Publisher ID: jcav06p0327
                DOI: 10.7150/jca.11185
                PMC ID: 4349872
                SO-VID: 688d9ff1-b2db-4c07-8ea7-bcf0459515d5
                Copyright © © 2015 Ivyspring International Publisher. Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. See http://ivyspring.com/terms for terms and conditions.
                History
                Date received : 26 November 2014
                Date accepted : 3 January 2015
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: curcumin,bik,caspase-9,caspase-3,apoptosis,squamous cell carcinoma,natural product,head and neck cancer
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: curcumin, bik, caspase-9, caspase-3, apoptosis, squamous cell carcinoma, natural product, head and neck cancer

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