Document Type
Article
Publication Date
6-16-2022
Abstract
The diverse repertoires of cellular mechanisms that progress certain cancer types are being uncovered by recent research and leading to more effective treatment options. Ovarian cancer (OC) is among the most difficult cancers to treat. OC has limited treatment options, especially for patients diagnosed with late-stage OC. The dysregulation of miRNAs in OC plays a significant role in tumorigenesis through the alteration of a multitude of molecular processes. The development of OC can also be due to the utilization of endogenously derived reactive oxygen species (ROS) by activating signaling pathways such as PI3K/AKT and MAPK. Both miRNAs and ROS are involved in regulating OC angiogenesis through mediating multiple angiogenic factors such as hypoxia-induced factor (HIF-1) and vascular endothelial growth factor (VEGF). The NAPDH oxidase subunit NOX4 plays an important role in inducing endogenous ROS production in OC. This review will discuss several important miRNAs, NOX4, and ROS, which contribute to therapeutic resistance in OC, highlighting the effective therapeutic potential of OC through these mechanisms.
Recommended Citation
Stieg, David C; Wang, Yifang; Liu, Ling-Zhi; and Jiang, Bing-Hua, "ROS and miRNA Dysregulation in Ovarian Cancer Development, Angiogenesis and Therapeutic Resistance" (2022). Kimmel Cancer Center Faculty Papers. Paper 92.
https://jdc.jefferson.edu/kimmelccfp/92
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
PubMed ID
35743145
Language
English
Included in
Medical Anatomy Commons, Medical Cell Biology Commons, Medical Pathology Commons, Oncology Commons
Comments
this article is the author's final published version in International Journal of Molecular Sciences, Volume 23, Issue 12, June 2022, Article number 6702.
The published version is available at https://doi.org/10.3390/ijms23126702.
Copyright © 2022 by the authors.
Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).