Kif14 overexpression accelerates murine retinoblastoma development

Michael O'Hare, Mehdi Shadmand, Rania S. Sulaiman, Kamakshi Sishtla, Toshiaki Sakisaka, Timothy W. Corson

Research output: Contribution to journalArticle

10 Scopus citations


The mitotic kinesin KIF14 has an essential role in the recruitment of proteins required for the final stages of cytokinesis. Genomic gain and/or overexpression of KIF14 has been documented in retinoblastoma and a number of other cancers, such as breast, lung and ovarian carcinomas, strongly suggesting its role as an oncogene. Despite evidence of oncogenic properties in vitro and in xenografts, Kif14's role in tumor progression has not previously been studied in a transgenic cancer model. Using a novel Kif14 overexpressing, simian virus 40 large T-antigen retinoblastoma (TAg-RB) double transgenic mouse model, we aimed to determine Kif14's role in promoting retinal tumor formation. Tumor initiation and development in double transgenics and control TAg-RB littermates were documented in vivo over a time course by optical coherence tomography, with subsequent ex vivo quantification of tumor burden. Kif14 overexpression led to an accelerated initiation of tumor formation in the TAg-RB model and a significantly decreased tumor doubling time (1.8 vs. 2.9 weeks). Moreover, overall percentage tumor burden was also increased by Kif14 overexpression. These data provide the first evidence that Kif14 can promote tumor formation in susceptible cells in vivo.

Original languageEnglish (US)
Pages (from-to)1752-1758
Number of pages7
JournalInternational Journal of Cancer
Issue number8
StatePublished - Oct 15 2016


  • kinesin
  • oncogene
  • optical coherence tomography
  • retinoblastoma
  • transgenic mouse

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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  • Cite this

    O'Hare, M., Shadmand, M., Sulaiman, R. S., Sishtla, K., Sakisaka, T., & Corson, T. W. (2016). Kif14 overexpression accelerates murine retinoblastoma development. International Journal of Cancer, 139(8), 1752-1758.