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

David C. Stieg & Bing-Hua Jiang et al. · 2022-06-16

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.

Funding
NIEHS NIH HHS Grant R01ES024151Mechanism of lung cancer resistance to tyrosine kinase inhibitor and radiation treatmentsMETTL3 in chromium-induced angiogenesis and carcinogenesisMiR-152/PKM2/SLC7A5 axis in breast cancer development, chemo- and radiation-treatment responseNew Mechanism of Arsenic CarcinogenesisAmerican Cancer Society Grant NEC-129306Pennsylvania Department of Health Grant SAP#41000Chromium in carcinogenesis and angiogenesisMechanism of lung cancer resistance to tyrosine kinase inhibitor and radiation treatmentsMETTL3 in chromium-induced angiogenesis and carcinogenesisMiR-152/PKM2/SLC7A5 axis in breast cancer development, chemo- and radiation-treatment responseNew Mechanism of Arsenic CarcinogenesisNational Institutes of Health Grant NEC-129306National Institutes of Health Grant SAP#41000Chromium in carcinogenesis and angiogenesisMechanism of lung cancer resistance to tyrosine kinase inhibitor and radiation treatmentsMETTL3 in chromium-induced angiogenesis and carcinogenesisMiR-152/PKM2/SLC7A5 axis in breast cancer development, chemo- and radiation-treatment responseNew Mechanism of Arsenic CarcinogenesisAmerican Cancer Society Research Grant SAP#41000Chromium in carcinogenesis and angiogenesisMechanism of lung cancer resistance to tyrosine kinase inhibitor and radiation treatmentsMETTL3 in chromium-induced angiogenesis and carcinogenesisMiR-152/PKM2/SLC7A5 axis in breast cancer development, chemo- and radiation-treatment responseNew Mechanism of Arsenic CarcinogenesisPennsylvania Department of Health Grant NEC-129306

NCI NIH HHS

R01CA232587

NIEHS NIH HHS

R01ES033197

NCI NIH HHS

R01CA263506

NIEHS NIH HHS

K02ES029119

National Institutes of Health

R01ES027901

National Institutes of Health

R01CA232587

National Institutes of Health

R01ES033197

National Institutes of Health

R01CA263506

National Institutes of Health

K02ES029119

American Cancer Society Research

R01ES027901

American Cancer Society Research

R01CA232587

American Cancer Society Research

R01ES033197

American Cancer Society Research

R01CA263506

American Cancer Society Research

K02ES029119

Pennsylvania Department of Health

R01ES027901

Pennsylvania Department of Health

R01CA232587

Pennsylvania Department of Health

R01ES033197

Pennsylvania Department of Health

R01CA263506

Pennsylvania Department of Health

K02ES029119