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The human lncRNA LINC-PINT inhibits tumor cell invasion through a highly conserved sequence element

Oskar Marín-Béjar1,2,3, Aina M Mas1,2, Jovanna González1,2

  • 1Department of Gene Therapy and Regulation of Gene Expression, Center for Applied Medical Research, University of Navarra, Pamplona, 31008, Spain.

Genome Biology
|October 29, 2017
PubMed
Abstract

Insights

The long non-coding RNA LINC-PINT suppresses cancer invasion by interacting with PRC2. This interaction is crucial for repressing genes that promote cancer cell invasion, highlighting a conserved mechanism in cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genomics

Background:

  • The majority of cellular transcripts are non-coding RNAs, including long non-coding RNAs (lncRNAs).
  • Aberrant lncRNA expression is observed in cancer, with some implicated in cell transformation, though mechanisms remain unclear.
  • The sequence-function relationship of lncRNAs in cancer is largely unknown.

Purpose of the Study:

  • To investigate the function of the p53-regulated human lncRNA LINC-PINT in cancer.
  • To elucidate the molecular mechanisms underlying LINC-PINT's role in tumor suppression.
  • To identify conserved functional elements within LINC-PINT.

Main Methods:

  • Characterization of LINC-PINT expression in various cancer types.
  • Functional assays to assess LINC-PINT's impact on cancer cell invasiveness.
  • Cross-species sequence analysis to identify conserved functional elements.
  • Investigation of LINC-PINT's interaction with Polycomb Repressive Complex 2 (PRC2).
  • Analysis of LINC-PINT's effect on EGR1-regulated gene expression.

Main Results:

  • LINC-PINT is downregulated in multiple cancer types, acting as a tumor suppressor.
  • LINC-PINT reduces the invasive phenotype of cancer cells.
  • A conserved sequence element in LINC-PINT is essential for its tumor-suppressive function.
  • This element mediates a specific interaction with PRC2.
  • LINC-PINT-PRC2 interaction represses EGR1-regulated pro-invasion genes.

Conclusions:

  • LINC-PINT and PRC2 exhibit a conserved functional co-dependence.
  • A novel mechanism is proposed where LINC-PINT regulates PRC2 availability at specific genomic loci.
  • This lncRNA-mediated regulation impacts cancer cell invasion and progression.
Keywords:
CancerCell invasionEpigenetic regulationLncRNAPRC2

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