Inhibition of NADPH Oxidase-ROS Signal using Hyaluronic Acid Nanoparticles for Overcoming Radioresistance in Cancer Therapy

Upregulation of NADPH oxidases (NOXs) in cancer cells leads to chronic increase in intracellular reactive oxygen species (ROS) and adaptation to a high ROS level for cell survival and, thereby, low sensitivity to radiotherapy. To overcome resistance to radiotherapy, we have developed a bioactive and...

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Published inACS nano Vol. 16; no. 11; pp. 18708 - 18728
Main Authors Zhu, Lei, Zhao, Yi, Liu, Tongrui, Chen, Minglong, Qian, Wei Ping, Jiang, Binghua, Barwick, Benjamin G., Zhang, Lumeng, Styblo, Toncred M, Li, Xiaoxian, Yang, Lily
Format Journal Article
LanguageEnglish
Published United States American Chemical Society 22.11.2022
Subjects
Animals
Breast Neoplasms - drug therapy
Breast Neoplasms - radiotherapy
Female
Humans
Hyaluronic Acid - therapeutic use
Mice
Mice, Nude
NADPH Oxidases - genetics
NADPH Oxidases - metabolism
Nanoparticles
Radiation Tolerance
Reactive Oxygen Species - metabolism
hyaluronic acid nanoparticle (HANP)
targeted cancer therapy
NADPH oxidases
reactive oxygen species
radiotherapy resistance
GKT831
Redox imbalance
Online AccessGet full text
ISSN1936-0851
1936-086X
1936-086X
DOI10.1021/acsnano.2c07440

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Abstract Upregulation of NADPH oxidases (NOXs) in cancer cells leads to chronic increase in intracellular reactive oxygen species (ROS) and adaptation to a high ROS level for cell survival and, thereby, low sensitivity to radiotherapy. To overcome resistance to radiotherapy, we have developed a bioactive and CD44 targeted hyaluronic acid nanoparticle encapsulated with an NOX inhibitor, GKT831 (HANP/GKT831). We found that HANP/GKT831 had stronger inhibitory effects on ROS generation and cell proliferation than that of GKT831 alone in cancer cells. Systemic delivery of HANP/GKT831 led to the targeted accumulation in breast cancer patient derived xenograft (PDX) tumors in nude mice. Importantly, the combination of systemic delivery of HANP/GKT831 with a low dose of local radiotherapy significantly enhanced tumor growth inhibition in breast cancer PDX models. Our results showed that HANP/GKT831 primed tumor cells to radiation-induced DNA damage and cell death by downregulation of DNA repair function and oncogenic signal pathways.
AbstractList Upregulation of NADPH oxidases (NOXs) in cancer cells leads to chronic increase in intracellular reactive oxygen species (ROS) and adaptation to a high ROS level for cell survival and, thereby, low sensitivity to radiotherapy. To overcome resistance to radiotherapy, we have developed a bioactive and CD44 targeted hyaluronic acid nanoparticle encapsulated with an NOX inhibitor, GKT831 (HANP/GKT831). We found that HANP/GKT831 had stronger inhibitory effects on ROS generation and cell proliferation than that of GKT831 alone in cancer cells. Systemic delivery of HANP/GKT831 led to the targeted accumulation in breast cancer patient derived xenograft (PDX) tumors in nude mice. Importantly, the combination of systemic delivery of HANP/GKT831 with a low dose of local radiotherapy significantly enhanced tumor growth inhibition in breast cancer PDX models. Our results showed that HANP/GKT831 primed tumor cells to radiation-induced DNA damage and cell death by downregulation of DNA repair function and oncogenic signal pathways.
Upregulation of NADPH oxidases (NOXs) in cancer cells leads to chronic increase in intracellular reactive oxygen species (ROS) and adaptation to a high ROS level for cell survival and, thereby, low sensitivity to radiotherapy. To overcome resistance to radiotherapy, we have developed a bioactive and CD44 targeted hyaluronic acid nanoparticle encapsulated with an NOX inhibitor, GKT831 (HANP/GKT831). We found that HANP/GKT831 had stronger inhibitory effects on ROS generation and cell proliferation than that of GKT831 alone in cancer cells. Systemic delivery of HANP/GKT831 led to the targeted accumulation in breast cancer patient derived xenograft (PDX) tumors in nude mice. Importantly, the combination of systemic delivery of HANP/GKT831 with a low dose of local radiotherapy significantly enhanced tumor growth inhibition in breast cancer PDX models. Our results showed that HANP/GKT831 primed tumor cells to radiation-induced DNA damage and cell death by downregulation of DNA repair function and oncogenic signal pathways.Upregulation of NADPH oxidases (NOXs) in cancer cells leads to chronic increase in intracellular reactive oxygen species (ROS) and adaptation to a high ROS level for cell survival and, thereby, low sensitivity to radiotherapy. To overcome resistance to radiotherapy, we have developed a bioactive and CD44 targeted hyaluronic acid nanoparticle encapsulated with an NOX inhibitor, GKT831 (HANP/GKT831). We found that HANP/GKT831 had stronger inhibitory effects on ROS generation and cell proliferation than that of GKT831 alone in cancer cells. Systemic delivery of HANP/GKT831 led to the targeted accumulation in breast cancer patient derived xenograft (PDX) tumors in nude mice. Importantly, the combination of systemic delivery of HANP/GKT831 with a low dose of local radiotherapy significantly enhanced tumor growth inhibition in breast cancer PDX models. Our results showed that HANP/GKT831 primed tumor cells to radiation-induced DNA damage and cell death by downregulation of DNA repair function and oncogenic signal pathways.
Author Zhu, Lei
Liu, Tongrui
Styblo, Toncred M
Zhang, Lumeng
Zhao, Yi
Chen, Minglong
Li, Xiaoxian
Yang, Lily
Qian, Wei Ping
Barwick, Benjamin G.
Jiang, Binghua
AuthorAffiliation Department of Surgery and Winship Cancer Institute
Department of Nuclear Medicine, China-Japan Union Hospital
Department of Pathology and Laboratory Medicine
Department of Hematology and Medical Oncology
Emory University School of Medicine
Department of Pathology, Anatomy and Cell Biology
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Keywords hyaluronic acid nanoparticle (HANP)
targeted cancer therapy
NADPH oxidases
reactive oxygen species
radiotherapy resistance
GKT831
Redox imbalance
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Snippet Upregulation of NADPH oxidases (NOXs) in cancer cells leads to chronic increase in intracellular reactive oxygen species (ROS) and adaptation to a high ROS...
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SubjectTerms Animals
Breast Neoplasms - drug therapy
Breast Neoplasms - radiotherapy
Female
Humans
Hyaluronic Acid - therapeutic use
Mice
Mice, Nude
NADPH Oxidases - genetics
NADPH Oxidases - metabolism
Nanoparticles
Radiation Tolerance
Reactive Oxygen Species - metabolism
Title Inhibition of NADPH Oxidase-ROS Signal using Hyaluronic Acid Nanoparticles for Overcoming Radioresistance in Cancer Therapy
URI http://dx.doi.org/10.1021/acsnano.2c07440
https://www.ncbi.nlm.nih.gov/pubmed/36256454
https://www.proquest.com/docview/2725649906
Volume 16
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