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Cyclin D1b overexpression inhibits cell proliferation and induces cell apoptosis in cervical cancer cells in vitro and in vivo.

Abstract
Cyclin D1b is one of two proteins translated from cyclin D1 transcripts (isoforms a and b) that are generated due to gene polymorphism. Our previous study has reported low cyclin D1b expression in cervical cancer tissue, with an expression level in moderately or poorly differentiated tissues that was significantly lower than that in well-differentiated tissues. However, the functional role of cyclin D1b in cervical cancer remains to be elucidated. In this study, using a cervical cancer cell line with stable expression of cyclin D1b, we found that upregulation of cyclin D1b initiated cell cycle arrest at the G0/G1 phase and induced apoptosis, thereby inhibiting cell proliferation and colony formation. Furthermore, xenograft transplantation experiments in nude mice demonstrated that cyclin D1b upregulation inhibited cancer growth and induce apoptosis in vivo. In conclusion, the present study indicates anti-tumor effects of cyclin D1b in cervical cancer, suggesting that cyclin D1b may represent a potential therapeutic target for cervical cancer.
AuthorsNing Wang, Heng Wei, Duo Yin, Yanming Lu, Yao Zhang, Di Jiang, Yan Jiang, Shulan Zhang
JournalInternational journal of clinical and experimental pathology (Int J Clin Exp Pathol) Vol. 7 Issue 7 Pg. 4016-23 ( 2014) ISSN: 1936-2625 [Electronic] United States
PMID25120779 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Protein Isoforms
  • Cyclin D1
Topics
  • Animals
  • Apoptosis (physiology)
  • Blotting, Western
  • Cell Proliferation (physiology)
  • Cyclin D1 (genetics, metabolism)
  • Female
  • Flow Cytometry
  • HeLa Cells
  • Heterografts
  • Humans
  • In Situ Nick-End Labeling
  • In Vitro Techniques
  • Mice
  • Mice, Nude
  • Protein Isoforms (genetics, metabolism)
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Uterine Cervical Neoplasms (genetics, metabolism, pathology)

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