Induction of growth arrest and polycomb gene expression by reversine allows C2C12 cells to be reprogrammed to various differentiated cell types

Sze Wan Shan, Mei Kuen Tang, Pak Ham Chow, Miguel Maroto, Dong Qing Cai, Kenneth K. H. Lee

    Research output: Contribution to journalArticlepeer-review

    21 Citations (Scopus)

    Abstract

    Reversine is a small, cell permeable synthetic chemical that has the ability to reprogram C2C12 myogenic cells to become various differentiated cell types. However, we still do not know how reversine works or the genes and proteins involved. Hence, we have used comparative proteomic techniques to address this issue. We have identified several proteins that were associated with cell cycle progression which were downregulated by reversine. Simultaneously, there were proteins associated with the induction of growth arrest that were upregulated. Consequently, we investigated the effects of reversine on C2C12 cell growth and established that it inhibited cell growth. Reversine had little affects on cell survival. We also investigated whether expressions of the polycomb genes, polycomb repressive complex 1 (PHC1) and Ezh2, were affected by reversine. Polycomb group genes are normally involved in chromatin based gene silencing. We found that PHC1 and Ezh2 expressions were enhanced by reversine and that it correlated with the inhibition of muscle specific transcriptional factor genes, myogenin, MyoD, and Myf5. Therefore, we believe that reversine is able to reprogram C2C12 cells to various differentiated cell types by inducing cell growth arrest, and promoting PHC1 and Ezh2 expressions.

    Original languageEnglish
    Pages (from-to)4303-4316
    Number of pages14
    JournalProteomics
    Volume7
    Issue number23
    DOIs
    Publication statusPublished - Dec 2007

    Keywords

    • C2C12 cells
    • Growth arrest
    • Reversine
    • Transdifferentiation
    • Skeletal muscle differntiation
    • Multipotent stem cells
    • In vitro
    • Identification
    • Calreticulin
    • Withdrawal
    • Cycle
    • P53

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