The involvement of MCT-1 oncoprotein in inducing mitotic catastrophe and nuclear abnormalities

Hung Ju Shih, Kang Lin Chu, Meng Hsun Wu, Pei Hsuan Wu, Wei Wen Chang, Jan Show Chu, Lily Hui Ching Wang, Hideki Takeuchi, Toru Ouchi, Hsin Ling Hsu

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Centrosome amplification and chromosome abnormality are frequently identified in neoplasia and tumorigenesis. However, the mechanisms underlying these defects remain unclear. Here, we identify that MCT-1 is a centrosomal oncoprotein involved in mitosis. Knockdown of MCT-1 protein results in intercellular bridging, chromosome miscongregation, cytokinesis delay and mitotic death. Introduction of MCT-1 oncogene into the p53 deficient cells (MCT-1-p53), the mitotic checkpoint kinases and proteins are deregulated synergistically. These biochemical alterations are accompanied with increased frequencies of cytokinesis failure, multi-nucleation and centrosome amplification in subsequent cell cycle. As a result, the incidences of polyploidy and aneuploidy are progressively induced by prolonged cell cultivation or further promoted by sustained spindle damage on MCT-1-p53 background. These data show that the oncoprotein perturbs centrosome structure and mitotic progression, which provide the molecular aspect of chromsomal abnormality in vitro and the information for understanding the stepwise progression of tumors under oncogenic stress.

Original languageEnglish
Pages (from-to)934-952
Number of pages19
JournalCell Cycle
Volume11
Issue number5
DOIs
Publication statusPublished - Mar 1 2012

Keywords

  • Centrosome
  • Cytokinesis
  • MCT-1
  • Mitosis
  • Nuclear abnormalities
  • p53

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

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  • Cite this

    Shih, H. J., Chu, K. L., Wu, M. H., Wu, P. H., Chang, W. W., Chu, J. S., Wang, L. H. C., Takeuchi, H., Ouchi, T., & Hsu, H. L. (2012). The involvement of MCT-1 oncoprotein in inducing mitotic catastrophe and nuclear abnormalities. Cell Cycle, 11(5), 934-952. https://doi.org/10.4161/cc.11.5.19452