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REV1 Inhibition Enhances Radioresistance and Autophagy.

Kanayo E Ikeh1, Erica N Lamkin1, Andrew Crompton1

  • 1Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, VT 05405, USA.

Cancers
|November 13, 2021
PubMed
Summary
This summary is machine-generated.

Inhibiting the translesion synthesis (TLS) protein REV1 does not enhance cancer cell response to radiation. Instead, REV1 inhibition triggers autophagy, a marker of radioresistance, impacting cancer treatment strategies.

Keywords:
REV1autophagyetoposideionizing radiationsradioresistancetranslesion synthesis

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Area of Science:

  • Oncology
  • Molecular Biology
  • Radiation Oncology

Background:

  • Cancer therapy resistance remains a significant clinical hurdle.
  • Inhibition of the translesion synthesis (TLS) protein REV1 enhances chemotherapy response by inducing senescence.
  • The effect of REV1 inhibition on radiosensitivity is currently unknown.

Purpose of the Study:

  • To investigate whether REV1 inhibition sensitizes cancer cells to ionizing radiation.
  • To explore the underlying mechanisms of REV1's role in response to radiation therapy.

Main Methods:

  • Utilized small molecule inhibitors targeting REV1.
  • Exposed cancer cells to ionizing radiation.
  • Assessed cell response, senescence, and autophagy markers.

Main Results:

  • REV1 inhibition failed to radiosensitize cancer cells.
  • REV1 inhibition unexpectedly induced autophagy, a known radioresistance biomarker.
  • This suggests REV1's role in treatment outcome is DNA damage-dependent.

Conclusions:

  • REV1 inhibition does not improve outcomes for radiation therapy.
  • REV1 inhibition triggers autophagy, an uncharacterized phenotype with implications for cancer treatment.
  • REV1's function in cancer treatment may vary based on the type of DNA damage incurred.