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Nuclear endonuclease G controls cell proliferation in ovarian cancer

Ye Na Choi1, Tae Woong Seo1, Yui Taek Lee1

  • 1Department of Biology, Kyung Hee University, Seoul, South Korea.

FEBS Open Bio
|February 3, 2023
PubMed

Insights

Endonuclease G does not cause cell death in ovarian cancer but influences proliferation. Targeting this enzyme may offer new therapeutic strategies for ovarian cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ovarian cancer exhibits significant genetic heterogeneity.
  • Current treatments like chemotherapy have limited efficacy due to toxicity and recurrence.
  • Identifying novel therapeutic targets is crucial for improving ovarian cancer treatment outcomes.

Purpose of the Study:

  • To investigate the role of endonuclease G in ovarian cancer.
  • To determine if endonuclease G functions as a cell death effector in ovarian cancer.
  • To explore the potential of targeting endonuclease G as a therapeutic strategy.

Main Methods:

  • Analysis of endonuclease G expression in ovarian cancer.
  • Investigation of endonuclease G's function in relation to cell death and DNA digestion.
  • Assessment of the modulation of endonuclease G by reactive oxygen species.
  • Evaluation of endonuclease G's role in ovarian cancer cell proliferation.

Main Results:

  • Endonuclease G expression is altered in ovarian cancer.
  • Endonuclease G does not function as a cell death effector by digesting chromosomal DNA in ovarian cancer.
  • Endonuclease G activity is modulated by intracellular reactive oxygen species dynamics.
  • Endonuclease G plays a role in ovarian cancer cell proliferation.

Conclusions:

  • Endonuclease G's role in ovarian cancer is not as a DNA-degrading cell death effector.
  • Endonuclease G's involvement in proliferation, modulated by reactive oxygen species, presents a potential therapeutic target.
  • Targeting endonuclease G, alone or in combination, may offer a novel treatment approach for ovarian cancer and other cancers with high endonuclease G expression.
Keywords:
antioxidantscell deathcell proliferationendonuclease G (EndoG)ovarian cancer (OC)reactive oxygen species (ROS)

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