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      Isocorydine Inhibits Cell Proliferation in Hepatocellular Carcinoma Cell Lines by Inducing G2/M Cell Cycle Arrest and Apoptosis

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          Abstract

          The treatment of human hepatocellular carcinoma (HCC) cell lines with (+)-isocorydine, which was isolated and purified from Papaveraceae sp. plants, resulted in a growth inhibitory effect caused by the induction of G2/M phase cell cycle arrest and apoptosis. We report that isocorydine induces G2/M phase arrest by increasing cyclin B1 and p-CDK1 expression levels, which was caused by decreasing the expression and inhibiting the activation of Cdc25C. The phosphorylation levels of Chk1 and Chk2 were increased after ICD treatment. Furthermore, G2/M arrest induced by ICD can be disrupted by Chk1 siRNA but not by Chk2 siRNA. In addition, isocorydine treatment led to a decrease in the percentage of CD133 + PLC/PRF/5 cells. Interestingly, isocorydine treatment dramatically decreased the tumorigenicity of SMMC-7721 and Huh7 cells. These findings indicate that isocorydine might be a potential therapeutic drug for the chemotherapeutic treatment of HCC.

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          Cancer Statistics, 2008

          A. Jemal, R. Siegel, E. Ward … (2008)
          Each year, the American Cancer Society 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. Incidence and death rates are age-standardized to the 2000 US standard million population. A total of 1,437,180 new cancer cases and 565,650 deaths from cancer are projected to occur in the United States in 2008. Notable trends in cancer incidence and mortality include stabilization of incidence rates for all cancer sites combined in men from 1995 through 2004 and in women from 1999 through 2004 and a continued decrease in the cancer death rate since 1990 in men and since 1991 in women. Overall cancer death rates in 2004 compared with 1990 in men and 1991 in women decreased by 18.4% and 10.5%, respectively, resulting in the avoidance of over a half million deaths from cancer during this time interval. This report also examines cancer incidence, mortality, and survival by site, sex, race/ethnicity, education, geographic area, and calendar year, as well as the proportionate contribution of selected sites to the overall trends. Although much progress has been made in reducing mortality rates, stabilizing incidence 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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            Identification of selective inhibitors of cancer stem cells by high-throughput screening.

            Piyush B Gupta, Tamer Onder, Guozhi Jiang … (2009)
            Screens for agents that specifically kill epithelial cancer stem cells (CSCs) have not been possible due to the rarity of these cells within tumor cell populations and their relative instability in culture. We describe here an approach to screening for agents with epithelial CSC-specific toxicity. We implemented this method in a chemical screen and discovered compounds showing selective toxicity for breast CSCs. One compound, salinomycin, reduces the proportion of CSCs by >100-fold relative to paclitaxel, a commonly used breast cancer chemotherapeutic drug. Treatment of mice with salinomycin inhibits mammary tumor growth in vivo and induces increased epithelial differentiation of tumor cells. In addition, global gene expression analyses show that salinomycin treatment results in the loss of expression of breast CSC genes previously identified by analyses of breast tissues isolated directly from patients. This study demonstrates the ability to identify agents with specific toxicity for epithelial CSCs.
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              Universal control mechanism regulating onset of M-phase.

              P Nurse (1990)
              The onset of M-phase is regulated by a mechanism common to all eukaryotic cells. Entry into M-phase is determined by activation of the p34cdc2 protein kinase which requires p34cdc2 dephosphorylation and association with cyclin.
              Article 0 comments Cited 252 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                : Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2012
                Publication date (Electronic): 18 May 2012
                Volume: 7
                Issue: 5
                Electronic Location Identifier: e36808
                Affiliations
                [1 ]State Key Laboratory of Oncogenes & Related Genes, Shanghai Cancer Institute, Renji Hospital, Jiaotong University School of Medicine, Shanghai, China
                [2 ]Experimental Pathological Laboratory, Shanghai Cancer Institute, Renji Hospital, Jiaotong University School of Medicine, Shanghai, China
                [3 ]College of Life Sciences and Chemistry, Tianshui Normal University, Tianshui, China
                The University of Hong Kong, China
                Author notes

                Conceived and designed the experiments: HS JL. Performed the experiments: HS HH PL LZ FZ CG MY. Analyzed the data: HS JL. Contributed reagents/materials/analysis tools: TW. Wrote the paper: HS JL. All authors were involved in writing the paper and had final approval of the submitted and published versions.

                Article
                Publisher ID: PONE-D-12-06024
                DOI: 10.1371/journal.pone.0036808
                PMC ID: 3356335
                PubMed ID: 22623962
                SO-VID: 10608676-d990-471e-8ce5-796174a9d015
                Copyright © Sun et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                Date received : 24 February 2012
                Date accepted : 6 April 2012
                Page count
                Pages: 11
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Biochemistry
                Subject: Drug Discovery
                Subject: Molecular Cell Biology
                Subject: Cytometry
                Subject: Flow Cytometry
                Subject: Cell Death
                Subject: Cell Growth
                Subject: Cellular Stress Responses
                Subject: Membranes and Sorting
                Subject: Chemistry
                Subject: Phytochemistry
                Subject: Phytopharmacology
                Subject: Medicine
                Subject: Oncology
                Subject: Cancers and Neoplasms
                Subject: Gastrointestinal Tumors
                Subject: Hepatocellular Carcinoma
                Subject: Basic Cancer Research

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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