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Nuclear retention of the lncRNA SNHG1 by doxorubicin attenuates hnRNPC-p53 protein interactions

Yuan Shen1,2, Shanshan Liu1,3, Jiao Fan1,4

  • 1Beijing Key Laboratory for Radiobiology, Beijing Institute of Radiation Medicine, Beijing, China.

EMBO Reports
|March 8, 2017
PubMed

Insights

The protein hnRNPC normally suppresses p53 activity. However, the lncRNA SNHG1 binding to hnRNPC upon doxorubicin treatment releases p53, promoting apoptosis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • RNA Biology

Background:

  • The tumor suppressor protein p53 regulates cellular stress responses.
  • Understanding p53 regulation mechanisms is crucial for cell biology.
  • The role of RNA in modulating protein interactions, including p53, requires further investigation.

Purpose of the Study:

  • To identify novel interactors of p53.
  • To elucidate the regulatory mechanisms of p53 activity by RNA.
  • To investigate the role of hnRNPC and SNHG1 in p53 regulation and apoptosis.

Main Methods:

  • Systematic experimental screening for p53 interactors.
  • Biochemical assays to determine direct binding and effects on protein stability.
  • Analysis of RNA-protein interactions and subcellular localization.
  • Assessment of p53-dependent apoptosis upon doxorubicin treatment.

Main Results:

  • hnRNPC directly binds to p53, destabilizing it and inhibiting its activation under normal conditions.
  • Doxorubicin treatment causes lncRNA SNHG1 to bind nucleolin, retaining it in the nucleus.
  • SNHG1 competes with p53 for hnRNPC binding, leading to p53 upregulation and apoptosis.
  • A balance between SNHG1 and hnRNPC regulates p53 activity and apoptosis.

Conclusions:

  • hnRNPC acts as a negative regulator of p53 under normal conditions.
  • lncRNA SNHG1 modulates p53 activity by sequestering hnRNPC upon doxorubicin treatment.
  • The subcellular localization and interaction dynamics of lncRNA SNHG1 are critical for p53-mediated apoptosis.
Keywords:
SNHG1doxorubicinhnRNPClncRNAp53

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