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Activity of roniciclib in medullary thyroid cancer

  • Shu Fu Lin*
  • , Jen Der Lin
  • , Chuen Hsueh
  • , Ting Chao Chou
  • , Richard J. Wong
  • *Corresponding author for this work
  • Chang Gung University
  • Memorial Sloan-Kettering Cancer Center
  • PD Science, Inc.

Research output: Contribution to journalJournal Article peer-review

20 Scopus citations

Abstract

Altered cyclin-dependent kinase activity is observed in many human malignancies. Cyclin-dependent kinases that promote cell cycle progression may be promising targets in the treatment of cancer. The therapeutic effects of roniciclib, a cyclindependent kinase inhibitor for medullary thyroid cancer were investigated in the present study. Roniciclib inhibited medullary thyroid cancer cell proliferation in a dose-dependent manner. Roniciclib induced caspase-3 activity and contributed to apoptosis. Cell cycle progression was arrested in the G2 phase. In vivo, roniciclib treatment retarded the growth of tumors of medullary thyroid cancer xenografts. In addition, roniciclib in combination with sorafenib was more effective than either single treatment in a xenograft model. No morbidity was observed in animals treated with single roniciclib therapy and combination treatment of roniciclib and sorafenib. These data provide a rationale for clinical assessment of using roniciclib in the treatment of patients with medullary thyroid cancer.

Original languageEnglish
Pages (from-to)28030-28041
Number of pages12
JournalOncotarget
Volume9
Issue number46
DOIs
StatePublished - 15 06 2018

Bibliographical note

Publisher Copyright:
©Lin et al.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Cyclin-dependent kinase
  • Medullary thyroid cancer
  • Roniciclib

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