Overexpression of Cas-Interacting Zinc finger protein (CIZ) suppresses proliferation and enhances expression of type I collagen gene in osteoblast-like MC3T3E1 cells

Koichi Furuya, Tetsuya Nakamoto, Zhong J. Shen, Kunikazu Tsuji, Akira Nifuji, Hisamaru Hirai, Masaki Noda

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Osteoblasts are the cells which form bone under the regulation not only by hormones and cytokines but also by ECM molecules via their attachment. To obtain insights into the role of intracellular signaling molecules operating to mediate the attachment-related regulation of osteoblastic functions, we investigated in osteoblast-like MC3T3E1 cells the effects of the overexpression of CIZ, a novel signaling protein which interacts with p130Cas. In MC3T3E1 cells, CIZ mRNA is expressed constitutively. Endogenous CIZ was localized in the MC3T3E1 cells with relatively high levels of accumulation at the attachment sites when the cells were cultured on fibronectin, collagen, or BSA. CIZ overexpression increased the number of adhesion plaques and reduced proliferation of the cells compared to that of control cells transfected with an empty vector. Furthermore, CIZ overexpression enhanced type I collagen mRNA expression, the most abundant constituent of bone matrix and a major product of osteoblasts. Analysis of the promoter region of type I collagen gene identified the presence of a consensus CIZ-binding sequence, which indeed conferred responsiveness to CIZ overexpression to a hererologous promoter. These data indicate that CIZ acts as a novel regulatory molecule in controlling osteoblastic function.

Original languageEnglish (US)
Pages (from-to)329-335
Number of pages7
JournalExperimental Cell Research
Volume261
Issue number2
DOIs
StatePublished - Dec 15 2000

Keywords

  • CIZ
  • Cas
  • Collagen
  • Gene expression
  • Osteoblasts
  • Proliferation

ASJC Scopus subject areas

  • Cell Biology

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