Apurinic/Apyrimidinic Endonuclease/Redox Effector Factor-1(APE/Ref-1): A Unique Target for the Prevention and Treatment of Human Melanoma

Yang, Sun; Meyskens, Frank L.

doi:10.1089/ars.2008.2226

Cited by 13 publications

(9 citation statements)

References 119 publications

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“…It is also well documented that elevated APE/Ref-1 is associated with chemo-and radio-resistance in a number of cellular systems. Recently, this group also suggested that APE/Ref-1 is involved in the regulation of metastasis produced by melanoma cells [125]. These studies suggested that, as an adaptive response induced by APE/Ref-1, this transcription factor besides efficiently repairs oxidative DNA damage, also regulates redox-sensitive signaling such as AP-1 and NF-κB, which are involved in melanoma genesis.…”

Section: Redox Signaling In Melanomamentioning

confidence: 97%

The Role of Oxidative Stress in Melanoma Development, Progression and Treatment

Melo¹,

Molognoni²,

Jasiulionis³

2013

Recent Advances in the Biology, Therapy and Management of Melanoma

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Section: Redox Signaling In Melanomamentioning

confidence: 97%

The Role of Oxidative Stress in Melanoma Development, Progression and Treatment

Melo¹,

Molognoni²,

Jasiulionis³

2013

Recent Advances in the Biology, Therapy and Management of Melanoma

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“…APE1/Ref-1 has also been shown to be associated with tumor resistance to both ionizing radiation and chemotherapy [ 123 – 125 ]. Consequently, APE/Ref-1 has emerged as a promising therapeutic target for cancer treatment [ 115 , 120 , 126 ].…”

Section: Cancer Redox Adaptationmentioning

confidence: 99%

The Tumorigenic Roles of the Cellular REDOX Regulatory Systems

Castaldo

Freitas

Conchinha

et al. 2015

Oxidative Medicine and Cellular Longevity

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The cellular REDOX regulatory systems play a central role in maintaining REDOX homeostasis that is crucial for cell integrity, survival, and proliferation. To date, a substantial amount of data has demonstrated that cancer cells typically undergo increasing oxidative stress as the tumor develops, upregulating these important antioxidant systems in order to survive, proliferate, and metastasize under these extreme oxidative stress conditions. Since a large number of chemotherapeutic agents currently used in the clinic rely on the induction of ROS overload or change of ROS quality to kill the tumor, the cancer cell REDOX adaptation represents a significant obstacle to conventional chemotherapy. In this review we will first examine the different factors that contribute to the enhanced oxidative stress generally observed within the tumor microenvironment. We will then make a comprehensive assessment of the current literature regarding the main antioxidant proteins and systems that have been shown to be positively associated with tumor progression and chemoresistance. Finally we will make an analysis of commonly used chemotherapeutic drugs that induce ROS. The current knowledge of cancer cell REDOX adaptation raises the issue of developing novel and more effective therapies for these tumors that are usually resistant to conventional ROS inducing chemotherapy.

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“…4 and 5). Four of the transcription factors that APE1 regulates (NF-κB, AP-1, Stat3 and HIF-1α [25, 37, 49, 50]) have been implicated in pancreatic cancer progression, resistance to therapy, and metastatic potential [51, 52]. A recent review indicates that those four transcription factors are key regulators of multiple signals in pancreatic cancer and provides strong evidence for investigating the effects of targeting transcription factors to kill pancreatic cancer cells [53].…”

Section: Ape1’s Varied Functionsmentioning

confidence: 99%

APE1/Ref-1Role in Redox Signaling: Translational Applications of Targeting the Redox Function of the DNA Repair/Redox Protein APE1/Ref-1

Kelley¹,

Georgiadis²,

Fishel

2012

CMP

150

176

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The heterogeneity of most cancers diminishes the treatment effectiveness of many cancer-killing regimens. Thus, treatments that hold the most promise are ones that block multiple signaling pathways essential to cancer survival. One of the most promising proteins in that regard is APE1, whose reduction-oxidation activity influences multiple cancer survival mechanisms, including growth, proliferation, metastasis, angiogenesis, and stress responses. With the continued research using APE1 redox specific inhibitors alone or coupled with developing APE1 DNA repair inhibitors it will now be possible to further delineate the role of APE1 redox, repair and protein-protein interactions. Previously, use of siRNA or over expression approaches, while valuable, do not give a clear picture of the two major functions of APE1 since both techniques severely alter the cellular milieu. Additionally, use of the redox-specific APE1 inhibitor, APX3330, now makes it possible to study how inhibition of APE1’s redox signaling can affect multiple tumor pathways and can potentiate the effectiveness of existing cancer regimens. Because APE1 is an upstream effector of VEGF, as well as other molecules that relate to angiogenesis and the tumor microenvironment, it is also being studied as a possible treatment for age-related macular degeneration and diabetic retinopathy. This paper reviews all of APE1’s functions, while heavily focusing on its redox activities. It also discusses APE1’s altered expression in many cancers and the therapeutic potential of selective inhibition of redox regulation, which is the subject of intense preclinical studies.

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Apurinic/Apyrimidinic Endonuclease/Redox Effector Factor-1(APE/Ref-1): A Unique Target for the Prevention and Treatment of Human Melanoma

Cited by 13 publications

References 119 publications

The Role of Oxidative Stress in Melanoma Development, Progression and Treatment

The Role of Oxidative Stress in Melanoma Development, Progression and Treatment

The Tumorigenic Roles of the Cellular REDOX Regulatory Systems

APE1/Ref-1Role in Redox Signaling: Translational Applications of Targeting the Redox Function of the DNA Repair/Redox Protein APE1/Ref-1

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