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RBM38 is a direct transcriptional target of E2F1 that limits E2F1-induced proliferation

Orit Feldstein1, Rotem Ben-Hamo, Dana Bashari

  • 1The Mina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan 52900, Israel. doron.ginsberg@biu.ac.il.

Molecular Cancer Research : MCR
|July 17, 2012
PubMed

Insights

The E2F1 transcription factor regulates RBM38, a protein that inhibits cell proliferation. This E2F1-RBM38 feedback loop restricts tumor growth and improves patient survival in ovarian cancer.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • The E2F/pRB pathway is crucial for cell proliferation control and frequently disrupted in human tumors.
  • The RNA-binding protein RBM38 (RNPC1) induces cell-cycle arrest by stabilizing p21 mRNA.
  • Altered RBM38 expression is observed in various cancers, with generally increased levels, but decreased in some breast tumors.

Purpose of the Study:

  • To investigate the regulatory relationship between E2F1 and RBM38.
  • To determine if RBM38 is a direct transcriptional target of E2F1.
  • To explore the functional implications of the E2F1-RBM38 interaction in cancer, particularly in ovarian cancer survival.

Main Methods:

  • Analysis of RBM38 mRNA and protein levels following E2F1 activation (exogenous and endogenous).
  • Chromatin immunoprecipitation (ChIP) to assess E2F1 binding to the RBM38 promoter.
  • E2F1 knockdown experiments to evaluate the effect on RBM38 expression.
  • Functional assays assessing cell-cycle progression upon RBM38 inhibition.
  • Correlation analysis of E2F1 and RBM38 expression with patient survival in ovarian cancer.

Main Results:

  • E2F1 activation leads to increased RBM38 mRNA and protein levels.
  • E2F1 directly binds to the human RBM38 promoter.
  • Knockdown of E2F1 reduces RBM38 expression.
  • Inhibition of RBM38 enhances E2F1-mediated cell-cycle progression.
  • High co-expression of E2F1 and RBM38 correlates with improved survival in ovarian cancer patients.

Conclusions:

  • RBM38 is identified as a novel transcriptional target of E2F1.
  • The E2F1-RBM38 interaction forms a negative feedback loop that restricts E2F1-driven proliferation.
  • This feedback loop plays a role in limiting tumor aggressiveness and enhancing patient survival, particularly in ovarian cancer.

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