Control of cell cycle regulatory proteins and modulation of STAT1 proteins by IFN-γ in human prostatic JCA-1 cells

M. Oya, S. Konno, Y. Chen, H. Tazaki, C. Mallouh, J. M. Wu

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


The addition of human recombinant IFN-γ (102 and 103 IU/ml) inhibited human prostatic JCA-1 cell growth by 27% and '64%, respectively. Since the high dose of IFN-γ elicited an increase in G1 concomitant with a decrease in G2/M phases of the cell cycle, changes in the expression of cell cycle regulatory protein molecules were analyzed by Western blots. Results of these experiments show that IFN-γ down regulated the G1/S transition molecules, e.g., cyclin D1, the cyclin-dependent protein kinase Cdk4, and the retinoblastoma gene product (pRB), but increased the G2/M transition molecules, e.g., cyclin B1 and p34cdc2 (Cdk1). Possible modulation of Cdk-inhibitors (CDKIs), e.g., p53 and p21WAF1 which have checkpoint functions in the cell cycle, by IFN-γ, was also studied. The p53 was induced by both 102 and 103 IU/ml IFN-γ. At 103 IU/ml, IFN-γ inhibited p21WAF1, increased the expression of STATlα, and sustained the elevated STAT1α for up to 96 h. Thus several mechanisms may be involved in the antiproliferative effects of IFN-γ.

Original languageEnglish
Pages (from-to)835-839
Number of pages5
JournalInternational journal of oncology
Issue number4
Publication statusPublished - 1997 Dec 1
Externally publishedYes


  • Cyclin-dependent kinase inhibitors
  • Cyclin-dependent kinases
  • Cyclins
  • IFN-
  • Prostate cancer
  • STAT1

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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