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Induction of p21(WAF1/CIP1) by human synovial sarcoma-associated chimeric oncoprotein SYT-SSX1

Masumi Tsuda1, Takuya Watanabe, Tatsuya Seki

  • 1Laboratory of Molecular and Cellular Pathology, Hokkaido University Graduate School of Medicine, N15, W7, Kita-ku, Sapporo 060-8638, Japan.

Oncogene
|August 17, 2005
PubMed

Insights

The chimeric oncoprotein SYT-SSX1 induces cell growth suppression by activating the p21 gene. This process is independent of hBRM and p53 but relies on Sp1/Sp3 transcription factors.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Oncogenic proteins can induce premature senescence, a cell cycle arrest mechanism.
  • Ras proteins are known to induce the cyclin-dependent kinase inhibitor p16(INK4A) in fibroblasts.
  • The role of SYT-SSX1 in senescence and cell cycle regulation is not fully understood.

Purpose of the Study:

  • To investigate the mechanism by which the human chimeric oncoprotein SYT-SSX1 suppresses cell growth.
  • To determine if SYT-SSX1 induces cell cycle inhibitors and to identify the specific pathways involved.

Main Methods:

  • Analysis of p21(WAF1/CIP1) (p21) expression and promoter activity in synovial sarcoma cell lines and human diploid fibroblasts.
  • Transient expression assays of SYT-SSX1 and its deletion mutants.
  • Reporter assays using wild-type and mutated p21 gene promoters.
  • Cell growth assays in SW13 cells stably expressing SYT-SSX1.

Main Results:

  • SYT-SSX1 induces the expression of cyclin-dependent kinase inhibitor p21(WAF1/CIP1) (p21), leading to cell growth suppression.
  • SYT-SSX1 activates the transcriptional activity of the p21 gene promoter.
  • p21 induction by SYT-SSX1 is independent of the chromatin remodeling factor hBRM and the tumor suppressor p53.
  • SYT-SSX1-mediated p21 induction is dependent on Sp1/Sp3 transcription factor binding sites within the p21 promoter.

Conclusions:

  • The human chimeric oncoprotein SYT-SSX1 suppresses cell growth by inducing p21.
  • SYT-SSX1 activates p21 transcription through Sp1/Sp3 binding sites, independent of hBRM and p53.
  • These findings elucidate a novel mechanism of oncogenesis involving SYT-SSX1 and p21 regulation.

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