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eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by novel small molecules.

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Hypoxia triggers cellular plasticity and metastasis via translation, not just transcription. Targeting eIF3e selectively inhibits this stress response, offering potential therapeutic avenues for cancer.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Stress Response

Background:

  • Hypoxia (low oxygen) promotes cancer cell plasticity and metastasis, primarily through transcriptional changes mediated by hypoxia-inducible factors (HIFs).
  • Translational regulation during hypoxia, which precedes transcriptional effects, remains understudied.
  • The role of translation initiation factors in hypoxia-induced cellular responses is largely unexplored.

Purpose of the Study:

  • To investigate the role of translational control in acute hypoxic responses.
  • To identify specific translation factors involved in hypoxia-induced cellular plasticity and metastasis.
  • To explore therapeutic strategies targeting hypoxia-induced translational reprogramming.

Main Methods:

  • Ribosome profiling to analyze global translation changes during acute hypoxia.
  • Functional assays to assess the impact of eIF3d/eIF3e on hypoxic responses and cancer cell invasion.
  • Analysis of eIF3e expression and copy number in breast cancer patient data.
  • Small molecule screening to identify inhibitors of eIF3e-mediated translation.

Main Results:

  • A selective translational response to acute hypoxia was identified, dependent on eukaryotic initiation factor 3 subunit d (eIF3d) and eIF3e.
  • This eIF3d/eIF3e-dependent translation controls key hypoxic responses, including HIF1a accumulation and cellular invasion.
  • Elevated eIF3e copy number and expression signatures correlate with poorer outcomes in breast cancer patients.
  • Novel small molecules targeting eIF3e were found to reduce hypoxia and ER stress-induced translation.

Conclusions:

  • The study uncovers critical roles for eIF3d/eIF3e in mediating cellular responses to hypoxia.
  • Targeting eIF3e presents a potential strategy to inhibit stress-induced translation, plasticity, and metastasis in cancer.
  • This work highlights translational control as a key mechanism in hypoxia-driven cancer progression.