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Article: Tissue-specific regulation of pregnane X receptor in cancer development and therapy.

Robbins, Delira / Chen, Taosheng

2014 Volume 4, Issue 1, Page(s) 17

Abstract: As a ligand-dependent transcription factor of the nuclear hormone receptor superfamily, the pregnane X receptor (PXR) has a multitude of functions including regulating xenobiotic and cholesterol metabolism, energy homeostasis, gut mucosal defense, and ... ...

Abstract	As a ligand-dependent transcription factor of the nuclear hormone receptor superfamily, the pregnane X receptor (PXR) has a multitude of functions including regulating xenobiotic and cholesterol metabolism, energy homeostasis, gut mucosal defense, and cancer development. Whereas the detoxification functions of PXR have been widely studied and well established, the role of PXR in cancer has become controversial. With more than 60% of non-prescription and prescription drugs being metabolized by cytochrome P450 enzyme 3A4 (CYP3A4), a transcriptional target of PXR, insights into the regulation of PXR during systemic administration of novel treatment modalities will lead to a better understanding of PXR function in the context of human disease. Previous studies have suggested that PXR activation decreases drug sensitivity and augments chemoresistance in certain colon cancers mainly through the upregulation of CYP3A4 and multidrug resistance protein-1 (MDR1). Later studies suggest that downregulation of PXR expression may be oncogenic in hormone-dependent breast and endometrial cancers by reducing estrogen metabolism via CYP3A4; thus, higher estradiol concentrations contribute to carcinogenesis. These results suggest a differential role of PXR in tumor growth regulation dependent on tissue type and tumor microenvironment. Here, we will summarize the various mechanisms utilized by PXR to induce its diverse effects on cancerous tissues. Moreover, current approaches will be explored to evaluate the exploitation of PXR-mediated pathways as a novel mechanistic approach to cancer therapy.
Language	English
Publishing date	2014-04-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2593367-X
ISSN	2045-3701
ISSN	2045-3701
DOI	10.1186/2045-3701-4-17
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Manganese superoxide dismutase in cancer prevention.

Robbins, Delira / Zhao, Yunfeng

Antioxidants & redox signaling

2013 Volume 20, Issue 10, Page(s) 1628–1645

Abstract: Significance: Cancer is the second leading cause of death in the United States. Considering the quality of life and treatment cost, the best way to fight against cancer is to prevent or suppress cancer development. Cancer is preventable as indicated by ... ...

Abstract	Significance: Cancer is the second leading cause of death in the United States. Considering the quality of life and treatment cost, the best way to fight against cancer is to prevent or suppress cancer development. Cancer is preventable as indicated by human papilloma virus (HPV) vaccination and tamoxifen/raloxifen treatment in breast cancer prevention. The activities of superoxide dismutases (SODs) are often lowered during early cancer development, making it a rational candidate for cancer prevention. Recent advances: SOD liposome and mimetics have been shown to be effective in cancer prevention animal models. They've also passed safety tests during early phase clinical trials. Dietary supplement-based SOD cancer prevention provides another opportunity for antioxidant-based cancer prevention. New mechanistic studies have revealed that SOD inhibits not only oncogenic activity, but also subsequent metabolic shifts during early tumorigenesis. Critical issues: Lack of sufficient animal model studies targeting specific cancers; and lack of clinical trials and support from pharmaceutical industries also hamper efforts in further advancing SOD-based cancer prevention. Future directions: To educate and obtain support from our society that cancer is preventable. To combine SOD-based therapeutics with other cancer preventive agents to obtain synergistic effects. To formulate a dietary supplementation-based antioxidant approach for cancer prevention. Lastly, targeting specific populations who are prone to carcinogens, which can trigger oxidative stress as the mechanism of carcinogenesis.
MeSH term(s)	Animals ; Anticarcinogenic Agents/pharmacology ; Anticarcinogenic Agents/therapeutic use ; Clinical Trials as Topic ; Curcumin/pharmacology ; Curcumin/therapeutic use ; Humans ; Mitochondria/metabolism ; Molecular Targeted Therapy ; Neoplasms/enzymology ; Neoplasms/pathology ; Neoplasms/prevention & control ; Oxidative Stress ; Superoxide Dismutase/physiology
Chemical Substances	Anticarcinogenic Agents ; Superoxide Dismutase (EC 1.15.1.1) ; superoxide dismutase 2 (EC 1.15.1.1) ; Curcumin (IT942ZTH98)
Language	English
Publishing date	2013-07-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2013.5297
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Article ; Online: Oxidative Stress Induced by MnSOD-p53 Interaction

Delira Robbins / Yunfeng Zhao

Journal of Signal Transduction, Vol

Pro- or Anti-Tumorigenic?

2012 Volume 2012

Abstract: The formation of reactive oxygen species (ROS) is a result of incomplete reduction of molecular oxygen during cellular metabolism. Although ROS has been shown to act as signaling molecules, it is known that these reactive molecules can act as prooxidants ...

Abstract	The formation of reactive oxygen species (ROS) is a result of incomplete reduction of molecular oxygen during cellular metabolism. Although ROS has been shown to act as signaling molecules, it is known that these reactive molecules can act as prooxidants causing damage to DNA, proteins, and lipids, which over time can lead to disease propagation and ultimately cell death. Thus, restoring the protective antioxidant capacity of the cell has become an important target in therapeutic intervention. In addition, a clearer understanding of the disease stage and molecular events that contribute to ROS generation during tumor promotion can lead to novel approaches to enhance target specificity in cancer progression. This paper will focus on not only the traditional routes of ROS generation, but also on new mechanisms via the tumor suppressor p53 and the interaction between p53 and MnSOD, the primary antioxidant enzyme in mitochondria. In addition, the potential consequences of the p53-MnSOD interaction have also been discussed. Lastly, we have highlighted clinical implications of targeting the p53-MnSOD interaction and discussed recent therapeutic mechanisms utilized to modulate both p53 and MnSOD as a method of tumor suppression.
Keywords	Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Hindawi Publishing Corporation
Document type	Article ; Online
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Article ; Online: Targeting xenobiotic receptors PXR and CAR in human diseases.

Banerjee, Monimoy / Robbins, Delira / Chen, Taosheng

Drug discovery today

2015 Volume 20, Issue 5, Page(s) 618–628

Abstract: Nuclear receptors such as the pregnane X receptor (PXR) and constitutive androstane receptor (CAR) are xenobiotic receptors regulating not only drug metabolism and disposition but also various human diseases such as cancer, diabetes, inflammatory disease, ...

Abstract	Nuclear receptors such as the pregnane X receptor (PXR) and constitutive androstane receptor (CAR) are xenobiotic receptors regulating not only drug metabolism and disposition but also various human diseases such as cancer, diabetes, inflammatory disease, metabolic disease and liver diseases, suggesting that PXR and CAR are promising targets for drug discovery. Consequently, there is an urgent need to discover and develop small molecules that target these PXR- and/or CAR-mediated human-disease-related pathways for relevant therapeutic applications. This review proposes approaches to target PXR and CAR, either individually or simultaneously, in the context of various human diseases, taking into consideration the structural differences between PXR and CAR.
MeSH term(s)	Binding Sites ; Biotransformation ; Drug Design ; Drug Interactions ; Humans ; Ligands ; Molecular Targeted Therapy ; Protein Binding ; Protein Conformation ; Receptor Cross-Talk ; Receptors, Cytoplasmic and Nuclear/chemistry ; Receptors, Cytoplasmic and Nuclear/drug effects ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Steroid/chemistry ; Receptors, Steroid/drug effects ; Receptors, Steroid/metabolism ; Signal Transduction/drug effects ; Structure-Activity Relationship
Chemical Substances	Ligands ; Receptors, Cytoplasmic and Nuclear ; Receptors, Steroid ; constitutive androstane receptor ; pregnane X receptor
Language	English
Publishing date	2015-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2014.11.011
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Article ; Online: The Role of Manganese Superoxide Dismutase in Skin Cancer

Delira Robbins / Yunfeng Zhao

Enzyme Research, Vol

2011 Volume 2011

Abstract: Recent studies have shown that antioxidant enzyme expression and activity are drastically reduced in most human skin diseases, leading to propagation of oxidative stress and continuous disease progression. However, antioxidants, an endogenous defense ... ...

Abstract	Recent studies have shown that antioxidant enzyme expression and activity are drastically reduced in most human skin diseases, leading to propagation of oxidative stress and continuous disease progression. However, antioxidants, an endogenous defense system against reactive oxygen species (ROS), can be induced by exogenous sources, resulting in protective effects against associated oxidative injury. Many studies have shown that the induction of antioxidants is an effective strategy to combat various disease states. In one approach, a SOD mimetic was applied topically to mouse skin in the two-stage skin carcinogenesis model. This method effectively reduced oxidative injury and proliferation without interfering with apoptosis. In another approach, Protandim, a combination of 5 well-studied medicinal plants, was given via dietary administration and significantly decreased tumor incidence and multiplicity by 33% and 57%, respectively. These studies suggest that alterations in antioxidant response may be a novel approach to chemoprevention. This paper focuses on how regulation of antioxidant expression and activity can be modulated in skin disease and the potential clinical implications of antioxidant-based therapies.
Keywords	Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Subject code	610
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The role of manganese superoxide dismutase in skin cancer.

Robbins, Delira / Zhao, Yunfeng

Enzyme research

2011 Volume 2011, Page(s) 409295

Abstract	Recent studies have shown that antioxidant enzyme expression and activity are drastically reduced in most human skin diseases, leading to propagation of oxidative stress and continuous disease progression. However, antioxidants, an endogenous defense system against reactive oxygen species (ROS), can be induced by exogenous sources, resulting in protective effects against associated oxidative injury. Many studies have shown that the induction of antioxidants is an effective strategy to combat various disease states. In one approach, a SOD mimetic was applied topically to mouse skin in the two-stage skin carcinogenesis model. This method effectively reduced oxidative injury and proliferation without interfering with apoptosis. In another approach, Protandim, a combination of 5 well-studied medicinal plants, was given via dietary administration and significantly decreased tumor incidence and multiplicity by 33% and 57%, respectively. These studies suggest that alterations in antioxidant response may be a novel approach to chemoprevention. This paper focuses on how regulation of antioxidant expression and activity can be modulated in skin disease and the potential clinical implications of antioxidant-based therapies.
Language	English
Publishing date	2011-03-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2573712-0
ISSN	2090-0414 ; 2090-0406
ISSN (online)	2090-0414
ISSN	2090-0406
DOI	10.4061/2011/409295
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Article ; Online: Oxidative Stress Induced by MnSOD-p53 Interaction: Pro- or Anti-Tumorigenic?

Robbins, Delira / Zhao, Yunfeng

Journal of signal transduction

2011 Volume 2012, Page(s) 101465

Abstract	The formation of reactive oxygen species (ROS) is a result of incomplete reduction of molecular oxygen during cellular metabolism. Although ROS has been shown to act as signaling molecules, it is known that these reactive molecules can act as prooxidants causing damage to DNA, proteins, and lipids, which over time can lead to disease propagation and ultimately cell death. Thus, restoring the protective antioxidant capacity of the cell has become an important target in therapeutic intervention. In addition, a clearer understanding of the disease stage and molecular events that contribute to ROS generation during tumor promotion can lead to novel approaches to enhance target specificity in cancer progression. This paper will focus on not only the traditional routes of ROS generation, but also on new mechanisms via the tumor suppressor p53 and the interaction between p53 and MnSOD, the primary antioxidant enzyme in mitochondria. In addition, the potential consequences of the p53-MnSOD interaction have also been discussed. Lastly, we have highlighted clinical implications of targeting the p53-MnSOD interaction and discussed recent therapeutic mechanisms utilized to modulate both p53 and MnSOD as a method of tumor suppression.
Language	English
Publishing date	2011-10-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2582328-0
ISSN	2090-1747 ; 2090-1739
ISSN (online)	2090-1747
ISSN	2090-1739
DOI	10.1155/2012/101465
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Article ; Online: New Aspects of Mitochondrial Uncoupling Proteins (UCPs) and Their Roles in Tumorigenesis

Yunfeng Zhao / Delira Robbins

International Journal of Molecular Sciences, Vol 12, Iss 8, Pp 5285-

2011 Volume 5293

Abstract: Uncoupling proteins (UCPs) belong to a family of mitochondrial carrier proteins that are present in the mitochondrial inner membrane. UCP1 was first identified followed by its two homologs, UCP2 and UCP3. The physiological functions of UCP include ... ...

Abstract	Uncoupling proteins (UCPs) belong to a family of mitochondrial carrier proteins that are present in the mitochondrial inner membrane. UCP1 was first identified followed by its two homologs, UCP2 and UCP3. The physiological functions of UCP include lowering mitochondrial membrane potential and dissipating metabolic energy as heat. However, UCP can be dysregulated and may contribute to the pathogenesis of metabolic disorders and obesity. Recent studies suggest that UCP also plays a role in neurodegenerative diseases and atherosclerosis. In addition, the widely expressed UCP, UCP2, has been shown to be upregulated in a number of aggressive human cancers. One mechanism of UCP2 upregulation in these cancers is due to oxidative stress, and elevated UCP2 in turn reduces oxidative stress, which provides a growth advantage for these cancers. Nevertheless, new studies suggest UCP2 may interact with oncogenes and tumor suppressor genes, providing a potential new mechanism of how UCP2 contributes to cancer development. In this review, the evidence supporting the role of UCPs in diseases other than diabetes and obesity, the reports on how UCP is regulated in cancer cells, and how UCP may regulate p53 will be discussed.
Keywords	mitochondrial uncoupling ; UCP2 ; cancer ; UCP2 regulation ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2011-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: New aspects of mitochondrial Uncoupling Proteins (UCPs) and their roles in tumorigenesis.

Robbins, Delira / Zhao, Yunfeng

International journal of molecular sciences

2011 Volume 12, Issue 8, Page(s) 5285–5293

Abstract	Uncoupling proteins (UCPs) belong to a family of mitochondrial carrier proteins that are present in the mitochondrial inner membrane. UCP1 was first identified followed by its two homologs, UCP2 and UCP3. The physiological functions of UCP include lowering mitochondrial membrane potential and dissipating metabolic energy as heat. However, UCP can be dysregulated and may contribute to the pathogenesis of metabolic disorders and obesity. Recent studies suggest that UCP also plays a role in neurodegenerative diseases and atherosclerosis. In addition, the widely expressed UCP, UCP2, has been shown to be upregulated in a number of aggressive human cancers. One mechanism of UCP2 upregulation in these cancers is due to oxidative stress, and elevated UCP2 in turn reduces oxidative stress, which provides a growth advantage for these cancers. Nevertheless, new studies suggest UCP2 may interact with oncogenes and tumor suppressor genes, providing a potential new mechanism of how UCP2 contributes to cancer development. In this review, the evidence supporting the role of UCPs in diseases other than diabetes and obesity, the reports on how UCP is regulated in cancer cells, and how UCP may regulate p53 will be discussed.
MeSH term(s)	Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Disease Susceptibility/metabolism ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Humans ; Ion Channels/genetics ; Ion Channels/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/metabolism ; Uncoupling Protein 1
Chemical Substances	Ion Channels ; Mitochondrial Proteins ; Tumor Suppressor Protein p53 ; UCP1 protein, human ; Uncoupling Protein 1
Language	English
Publishing date	2011-08-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms12085285
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Article ; Online: Imaging NF-κB signaling in mice for screening anticancer drugs.

Robbins, Delira / Zhao, Yunfeng

Methods in molecular biology (Clifton, N.J.)

2011 Volume 716, Page(s) 169–177

Abstract: The activation of NF-κB has been implicated in various forms of cancer. Thereafter, targeting NF-κB has been suggested for cancer therapy. Instant and accurate tools to monitor NF-κB activation are necessary for such drug screening. Currently, there are ... ...

Abstract	The activation of NF-κB has been implicated in various forms of cancer. Thereafter, targeting NF-κB has been suggested for cancer therapy. Instant and accurate tools to monitor NF-κB activation are necessary for such drug screening. Currently, there are various assays available to study NF-κB activation in vitro, however, techniques involving the imaging of NF-κB in vivo models remains limited. Male NF-κB-RE-luc (Oslo) mice from Xenogen Corporation (Alameda, California) provide a great model for studying and imaging anticancer drugs that target NF-κB signaling. In addition, the bioluminescent (LPTA) animal model DBA/1, BALB/C-Tg (NF-κB-RE-luc (Oslo)), carries a transgene containing three NF-κB response element sites from the Igk light chain promoter and modified firefly luciferase cDNA (Promega pGL-3). The reporter is inducible during inflammatory processes triggered by LPS and TNF-α. This model provides for the rapid study of transcriptional regulation of the NF-κB gene and the treatment of inflammatory diseases and cancer. Therefore, in this chapter, we will provide step-by-step methods on utilizing the NF-κB-RE-luc animal model. In addition, we will provide notes on effective compound administration and imaging strategies that have been proven effective in previous studies.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Drug Screening Assays, Antitumor/methods ; Gene Expression Regulation ; Luciferases/genetics ; Luminescence ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; NF-kappa B/genetics ; NF-kappa B/metabolism
Chemical Substances	Antineoplastic Agents ; NF-kappa B ; Luciferases (EC 1.13.12.-)
Language	English
Publishing date	2011
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-61779-012-6_10
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