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Related Experiment Video

Updated: Jan 7, 2026

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A transcriptional program mediating entry into cellular quiescence.

Helen Liu1, Adam S Adler, Eran Segal

  • 1Program in Epithelial Biology, Stanford University School of Medicine, Stanford, California, United States of America.

Plos Genetics
|June 15, 2007
PubMed
Summary
This summary is machine-generated.

Cellular quiescence, induced by serum deprivation (SD), involves distinct early transcriptional responses. Serum deprivation early response genes (SDERGs) are crucial for halting DNA synthesis and may act as novel tumor inhibitors.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Tissue homeostasis relies on balancing cell quiescence and division.
  • Serum stimulation (SS) is a known inducer of cell division, but the mechanisms of cellular quiescence induction, such as via serum deprivation (SD), are less understood.

Purpose of the Study:

  • To elucidate the transcriptional responses to serum deprivation (SD) and identify genes involved in inducing cellular quiescence.
  • To investigate the role of identified genes in DNA synthesis cessation and their potential as tumor suppressors.

Main Methods:

  • Genome-wide transcriptional profiling following serum stimulation (SS) and serum deprivation (SD).
  • Functional analysis of serum deprivation early response genes (SDERGs) in DNA synthesis.
  • Analysis of SDERG expression in human cancers and correlation with cancer progression.

Main Results:

  • Distinct early transcriptional programs are activated by SS and SD, converging on a shared late program.
  • Several serum deprivation early response genes (SDERGs), including SALL2 and MXI1, are essential for inhibiting DNA synthesis during SD.
  • SDERGs are frequently repressed in human cancers, and their repression correlates with increased cancer progression and mortality.

Conclusions:

  • Serum deprivation (SD) triggers a unique gene expression program involving specific early response genes (SDERGs).
  • SDERGs play a critical role in inducing cellular quiescence and halting DNA synthesis.
  • Repressed SDERGs in cancer suggest their potential function as novel tumor suppressors and predictive biomarkers for cancer progression.