scholarly journals High Mobility Group B Proteins, Their Partners, and Other Redox Sensors in Ovarian and Prostate Cancer

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Aida Barreiro-Alonso ◽  
Mónica Lamas-Maceiras ◽  
Esther Rodríguez-Belmonte ◽  
Ángel Vizoso-Vázquez ◽  
María Quindós ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Structural Changes ◽  
Molecular Mechanisms ◽  
High Mobility ◽  
High Mobility Group ◽  
Redox Sensor ◽  
Group B ◽  
Different Origins ◽  
Hmgb Proteins

Cancer cells try to avoid the overproduction of reactive oxygen species by metabolic rearrangements. These cells also develop specific strategies to increase ROS resistance and to express the enzymatic activities necessary for ROS detoxification. Oxidative stress produces DNA damage and also induces responses, which could help the cell to restore the initial equilibrium. But if this is not possible, oxidative stress finally activates signals that will lead to cell death. High mobility group B (HMGB) proteins have been previously related to the onset and progressions of cancers of different origins. The protein HMGB1 behaves as a redox sensor and its structural changes, which are conditioned by the oxidative environment, are associated with different functions of the protein. This review describes recent advances in the role of human HMGB proteins and other proteins interacting with them, in cancerous processes related to oxidative stress, with special reference to ovarian and prostate cancer. Their participation in the molecular mechanisms of resistance to cisplatin, a drug commonly used in chemotherapy, is also revised.

scholarly journals Paradoxical role of high mobility group box 1 in glioma: a suppressor or a promoter?

2017 ◽  
Author(s):  
Richard A. Seidu ◽  
Min Wu ◽  
Zhaoliang Su ◽  
Huaxi Xu
Keyword(s):  
Molecular Mechanisms ◽  
High Mobility ◽  
Treatment Resistance ◽  
High Mobility Group ◽  
Tissue Invasion ◽  
Self Sufficiency ◽  
Glycation End Products ◽  
And Migration ◽  
Proliferation And Migration

Gliomas represent 60% of primary intracranial brain tumors and 80% of all malignant types, with highest morbidity and mortality worldwide. Although glioma has been extensively studied, the molecular mechanisms underlying its pathology remain poorly understood. Clarification of the molecular mechanisms involved in their development and/or treatment resistance is highly required. High mobility group box 1 protein (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation and migration, through receptor for advanced glycation end products and toll like receptors in a number of cancers including gliomas. It is known that excessive release of HMGB1 in cancer leads to unlimited replicative potential, ability to develop blood vessels (angiogenesis), evasion of programmed cell death (apoptosis), self-sufficiency in growth signals, insensitivity to inhibitors of growth, inflammation, tissue invasion and metastasis. In this review we explore the mechanisms by which HMGB1 regulates apoptosis and autophagy in glioma. We also looked at how HMGB1 mediates glioma regression and promotes angiogenesis as well as possible signaling pathways with an attempt to provide potential therapeutic targets for the treatment of glioma.

scholarly journals High Mobility Group Box 1 (HMGB1) Activates an Autophagic Response to Oxidative Stress

2011 ◽  
Vol 15 (8) ◽  
pp. 2185-2195 ◽  
Author(s):  
Daolin Tang ◽  
Rui Kang ◽  
Kristen M. Livesey ◽  
Herbert J. Zeh ◽  
Michael T. Lotze
Keyword(s):  
Oxidative Stress ◽  
High Mobility ◽  
High Mobility Group

scholarly journals High-Mobility Group Box 1, Oxidative Stress, and Disease

2011 ◽  
Vol 14 (7) ◽  
pp. 1315-1335 ◽  
Author(s):  
Daolin Tang ◽  
Rui Kang ◽  
Herbert J. Zeh ◽  
Michael T. Lotze
Keyword(s):  
Oxidative Stress ◽  
High Mobility ◽  
High Mobility Group

scholarly journals A Systematic Nomenclature for the Redox States of High Mobility Group Box (HMGB) Proteins

2014 ◽  
Vol 20 (1) ◽  
pp. 135-137 ◽  
Author(s):  
Daniel J. Antoine ◽  
Helena Erlandsson Harris ◽  
Ulf Andersson ◽  
Kevin J. Tracey ◽  
Marco E. Bianchi
Keyword(s):  
High Mobility ◽  
High Mobility Group ◽  
Redox States ◽  
Systematic Nomenclature ◽  
Hmgb Proteins

scholarly journals Targeting High Mobility Group Box 1 in Subarachnoid Hemorrhage: A Systematic Review

2020 ◽  
Vol 21 (8) ◽  
pp. 2709 ◽  
Author(s):  
Sajjad Muhammad ◽  
Shafqat Rasul Chaudhry ◽  
Ulf Dietrich Kahlert ◽  
Martin Lehecka ◽  
Miikka Korja ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Brain Damage ◽  
Molecular Mechanisms ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
High Mobility ◽  
High Mobility Group ◽  
Endovascular Coiling ◽  
Pharmacological Interventions

Aneurysmal subarachnoid hemorrhage (aSAH) is a complex and potentially deadly disease. Neurosurgical clipping or endovascular coiling can successfully obliterate ruptured aneurysms in almost every case. However, despite successful interventions, the clinical outcomes of aSAH patients are often poor. The reasons for poor outcomes are numerous, including cerebral vasospasm (CVS), post-hemorrhagic hydrocephalus, systemic infections and delayed cerebral ischemia. Although CVS with subsequent cerebral ischemia is one of the main contributors to brain damage after aSAH, little is known about the underlying molecular mechanisms of brain damage. This review emphasizes the importance of pharmacological interventions targeting high mobility group box 1 (HMGB1)-mediated brain damage after subarachnoid hemorrhage (SAH) and CVS. We searched Pubmed, Ovid medline and Scopus for “subarachnoid hemorrhage” in combination with “HMGB1”. Based on these criteria, a total of 31 articles were retrieved. After excluding duplicates and selecting the relevant references from the retrieved articles, eight publications were selected for the review of the pharmacological interventions targeting HMGB1 in SAH. Damaged central nervous system cells release damage-associated molecular pattern molecules (DAMPs) that are important for initiating, driving and sustaining the inflammatory response following an aSAH. The discussed evidence suggested that HMGB1, an important DAMP, contributes to brain damage during early brain injury and also to the development of CVS during the late phase. Different pharmacological interventions employing natural compounds with HMGB1-antagonizing activity, antibody targeting of HMGB1 or scavenging HMGB1 by soluble receptors for advanced glycation end products (sRAGE), have been shown to dampen the inflammation mediated brain damage and protect against CVS. The experimental data suggest that HMGB1 inhibition is a promising strategy to reduce aSAH-related brain damage and CVS. Clinical studies are needed to validate these findings that may lead to the development of potential treatment options that are much needed in aSAH.

Nuclear matrix localization of high mobility group protein I(Y) in a transgenic mouse model for prostate cancer

2002 ◽  
Vol 88 (3) ◽  
pp. 599-608 ◽  
Author(s):  
Eddy S. Leman ◽  
Michael C. Madigan ◽  
Gisela Brünagel ◽  
Natsuki Takaha ◽  
Donald S. Coffey ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Nuclear Matrix ◽  
High Mobility ◽  
Transgenic Mouse Model ◽  
High Mobility Group ◽  
High Mobility Group Protein ◽  
Group Protein
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