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ROS and miRNA Dysregulation in Ovarian Cancer Development, Angiogenesis and Therapeutic Resistance

David C Stieg1, Yifang Wang2, Ling-Zhi Liu1

  • 1Department of Medical Oncology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA.

International Journal of Molecular Sciences
|June 24, 2022
PubMed

Insights

This review explores microRNAs (miRNAs) and reactive oxygen species (ROS) in ovarian cancer (OC). Understanding their roles in therapeutic resistance could lead to novel OC treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ovarian cancer (OC) presents significant treatment challenges, particularly in late stages.
  • MicroRNA (miRNA) dysregulation and reactive oxygen species (ROS) are implicated in OC development and progression.
  • Signaling pathways like PI3K/AKT and MAPK are activated by ROS, contributing to tumorigenesis.

Purpose of the Study:

  • To review the roles of specific miRNAs, NOX4, and ROS in ovarian cancer.
  • To elucidate their contribution to therapeutic resistance in OC.
  • To highlight potential therapeutic strategies targeting these mechanisms.

Main Methods:

  • Literature review of current research on miRNAs, NOX4, and ROS in OC.
  • Analysis of molecular mechanisms underlying OC progression and therapeutic resistance.
  • Discussion of angiogenic factors like HIF-1 and VEGF in OC.

Main Results:

  • miRNAs and ROS significantly influence OC tumorigenesis and angiogenesis.
  • NOX4 is a key mediator of ROS production in OC.
  • These factors contribute to therapeutic resistance in ovarian cancer.

Conclusions:

  • Targeting specific miRNAs and ROS pathways, including NOX4, shows promise for overcoming OC therapeutic resistance.
  • Further research into these mechanisms could yield effective new treatments for ovarian cancer.
  • Understanding miRNA and ROS interplay is crucial for advancing OC therapy.
Keywords:
HER3HIF1-αNOX4ROSVEGFangiogenesismiRNA dysregulationovarian cancertherapeutic resistance

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