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Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

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Computational inference of eIF4F complex function and structure in human cancers.

Su Wu1, Gerhard Wagner1

  • 1Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.

Proceedings of the National Academy of Sciences of the United States of America
|January 24, 2024
PubMed
Summary
This summary is machine-generated.

Cancer cells utilize distinct translation initiation pathways, including cap-dependent and cap-independent mechanisms involving eukaryotic initiation factors (eIFs). This study reveals gene amplifications and structural insights into these processes, impacting cancer survival.

Keywords:
cap-independent translation initiationcomputational analysiseIF3eeIF4F dysregulationeukaryotic initiation factor 4F (eIF4F)

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Structural Biology

Background:

  • Canonical translation initiation in eukaryotes relies on the eukaryotic initiation factor 4F (eIF4F) complex (eIF4G1, eIF4A1, eIF4E) for cap-dependent mRNA binding.
  • Alternative cap-independent translation initiation occurs via internal ribosome entry sites (IRESs), involving eIF4G1 and eIF4A1, and is crucial for cancer cells under stress.
  • The precise molecular mechanisms governing the selection of these initiation pathways in human cancers remain poorly understood.

Purpose of the Study:

  • To investigate gene copy number variations (CNVs) and expression patterns of translation initiation factors in human cancers.
  • To elucidate the structural basis of cap-dependent and cap-independent translation initiation mechanisms.
  • To understand the correlation between translation initiation factor alterations and cancer cell survival pathways.

Main Methods:

  • Analysis of gene copy number variations (CNVs) in The Cancer Genome Atlas (TCGA) tumor samples.
  • Correlation analysis of gene expression data for translation initiation factors and cancer cell survival pathways.
  • Structural modeling of the eIF4F complex using AlphaFold predictions for both cap-dependent and cap-independent initiation states.

Main Results:

  • Frequent amplification of translation initiation genes, particularly co-occurring gains in EIF4G1 and EIF3E, was observed across human cancers.
  • EIF4G1 amplification correlated with increased expression of cell cycle and lipogenesis genes, suggesting a role in cancer survival.
  • Structural modeling revealed distinct interaction modes of eIF4G1 with eIF4E and eIF4A1, differentiating cap-dependent and cap-independent initiation pathways.

Conclusions:

  • Alterations in translation initiation factor gene copy numbers and expression are prevalent in human cancers and linked to cancer cell survival.
  • The structural insights highlight how eIF4G1 modulates interactions with eIF4A1 and eIF4E to regulate distinct translation initiation mechanisms.
  • Understanding these pathways offers potential therapeutic targets for modulating translation in cancer.