Mitosis perturbation by MASTL depletion impairs the viability of thyroid tumor cells

Elena Cetti, Tiziana Di Marco, Giuseppe Mauro, Mara Mazzoni, Daniele Lecis, Emanuela Minna, Lucia Gioiosa, Silvia Brich, Sonia Pagliardini, Maria Grazia Borrello, Giancarlo Pruneri, Maria Chiara Anania, Angela Greco

Research output: Contribution to journalArticlepeer-review


Even if thyroid tumors are generally curable, a fraction will develop resistance to therapy and progress towards undifferentiated forms, whose treatment remains a demanding challenge. To identify potential novel targets for treatment of thyroid cancer, in a previous study using siRNA-mediated functional screening, we identified several genes that are essential for the growth of thyroid tumor, but not normal cells. Among the top-ranking hits, we found microtubule associated serine/threonine kinase-like (MASTL), which is known to play an essential role in mitosis regulation, and is also involved in the DNA damage response. Herein, we examine the effects of MASTL depletion on growth and viability of thyroid tumor cells. MASTL depletion impaired cell proliferation and increased the percentage of cells presenting nuclear anomalies, which are indicative of mitotic catastrophe. Furthermore, MASTL depletion was associated with enhanced DNA damage. All these effects eventually led to cell death, characterized by the presence of apoptotic markers. Moreover, MASTL depletion sensitized thyroid tumor cells to cisplatin. Our results demonstrate that MASTL represents vulnerability for thyroid tumor cells, which could be explored as a therapeutic target for thyroid cancer.

Original languageEnglish
Pages (from-to)362-372
Number of pages11
JournalCancer Letters
Publication statusPublished - Feb 1 2019


  • Mitotic catastrophe
  • Non-oncogene addiction
  • Target validation
  • Thyroid tumor cells

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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