Mechanisms and Therapeutic Interventions for Breast Cancer-Induced Fatigue and Mitochondrial Dysfunction

2021 ◽  
Author(s):  
David Andrew Stanton
Keyword(s):  
Breast Cancer ◽  
Mitochondrial Dysfunction ◽  
Therapeutic Interventions

scholarly journals Cellular and Molecular Players in the Interplay between Adipose Tissue and Breast Cancer

2021 ◽  
Vol 22 (3) ◽  
pp. 1359
Author(s):  
Francesca Reggiani ◽  
Paolo Falvo ◽  
Francesco Bertolini
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Metabolic Disorders ◽  
Current Knowledge ◽  
Therapeutic Interventions ◽  
Preclinical Research ◽  
The World ◽  
Adipose Cells

The incidence and severity of obesity are rising in most of the world. In addition to metabolic disorders, obesity is associated with an increase in the incidence and severity of a variety of types of cancer, including breast cancer (BC). The bidirectional interaction between BC and adipose cells has been deeply investigated, although the molecular and cellular players involved in these mechanisms are far from being fully elucidated. Here, we review the current knowledge on these interactions and describe how preclinical research might be used to clarify the effects of obesity over BC progression and morbidity, with particular attention paid to promising therapeutic interventions.

scholarly journals Mitochondrial Dysfunction in Atrial Fibrillation—Mechanisms and Pharmacological Interventions

2021 ◽  
Vol 10 (11) ◽  
pp. 2385
Author(s):  
Paweł Muszyński ◽  
Tomasz A. Bonda
Keyword(s):  
Atrial Fibrillation ◽  
Mitochondrial Dysfunction ◽  
Treatment Options ◽  
Therapeutic Interventions ◽  
Energy Deficit ◽  
Functional Changes ◽  
Electrical Instability ◽  
Ionic Fluxes ◽  
Prevention Methods ◽  
Invasive Techniques

Despite the enormous progress in the treatment of atrial fibrillation, mainly with the use of invasive techniques, many questions remain unanswered regarding the pathomechanism of the arrhythmia and its prevention methods. The development of atrial fibrillation requires functional changes in the myocardium that result from disturbed ionic fluxes and altered electrophysiology of the cardiomyocyte. Electrical instability and electrical remodeling underlying the arrhythmia may result from a cellular energy deficit and oxidative stress, which are caused by mitochondrial dysfunction. The significance of mitochondrial dysfunction in the pathogenesis of atrial fibrillation remains not fully elucidated; however, it is emphasized by the reduction of atrial fibrillation burden after therapeutic interventions improving the mitochondrial welfare. This review summarizes the mechanisms of mitochondrial dysfunction related to atrial fibrillation and current pharmacological treatment options targeting mitochondria to prevent or improve the outcome of atrial fibrillation.

scholarly journals Breast Cancer in Low- and Middle-Income Countries: An Emerging and Challenging Epidemic

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Arafat Tfayli ◽  
Sally Temraz ◽  
Rachel Abou Mrad ◽  
Ali Shamseddine
Keyword(s):  
Breast Cancer ◽  
Health Care ◽  
Low Income ◽  
Therapeutic Interventions ◽  
Low Income Countries ◽  
Middle Income ◽  
Major Health ◽  
Middle Income Countries ◽  
Low And Middle Income

Breast cancer is a major health care problem that affects more than one million women yearly. While it is traditionally thought of as a disease of the industrialized world, around 45% of breast cancer cases and 55% of breast cancer deaths occur in low and middle income countries. Managing breast cancer in low income countries poses a different set of challenges including access to screening, stage at presentation, adequacy of management and availability of therapeutic interventions. In this paper, we will review the challenges faced in the management of breast cancer in low and middle income countries.

scholarly journals Mitochondrial dysfunction in breast cancer cells prevents tumor growth

Cell Cycle ◽  
2012 ◽  
Vol 12 (1) ◽  
pp. 172-182 ◽  
Author(s):  
Rosa Sanchez-Alvarez ◽  
Ubaldo E. Martinez-Outschoorn ◽  
Rebecca Lamb ◽  
James Hulit ◽  
Anthony Howell ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Mitochondrial Dysfunction ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals Targeting Mitochondria as Therapeutic Strategy for Metabolic Disorders

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Daniela Sorriento ◽  
Antonietta Valeria Pascale ◽  
Rosa Finelli ◽  
Anna Lisa Carillo ◽  
Roberto Annunziata ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Mitochondrial Dysfunction ◽  
Small Molecules ◽  
Metabolic Disorders ◽  
Therapeutic Strategy ◽  
Cell Metabolism ◽  
Therapeutic Interventions ◽  
Mtdna Mutations ◽  
Pathological Conditions ◽  
Mitochondria Targeting

Mitochondria are critical regulator of cell metabolism; thus, mitochondrial dysfunction is associated with many metabolic disorders. Defects in oxidative phosphorylation, ROS production, or mtDNA mutations are the main causes of mitochondrial dysfunction in many pathological conditions such as IR/diabetes, metabolic syndrome, cardiovascular diseases, and cancer. Thus, targeting mitochondria has been proposed as therapeutic approach for these conditions, leading to the development of small molecules to be tested in the clinical scenario. Here we discuss therapeutic interventions to treat mitochondrial dysfunction associated with two major metabolic disorders, metabolic syndrome, and cancer. Finally, novel mechanisms of regulation of mitochondrial function are discussed, which open new scenarios for mitochondria targeting.

Mitochondrial Dysfunction in Breast Cancer

2019 ◽  
pp. 103-114
Author(s):  
Thalita Basso Scandolara ◽  
Letícia Madureira Pacholak ◽  
Thayse Fachin Cormanique ◽  
Rodrigo Kern ◽  
Carolina Panis
Keyword(s):  
Breast Cancer ◽  
Mitochondrial Dysfunction

scholarly journals The Regulatory Role of Mitochondrial MicroRNAs (MitomiRs) in Breast Cancer: Translational Implications Present and Future

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2443 ◽  
Author(s):  
Miguel A. Ortega ◽  
Oscar Fraile-Martínez ◽  
Luis G. Guijarro ◽  
Carlos Casanova ◽  
Santiago Coca ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mitochondrial Dysfunction ◽  
Survival Rates ◽  
Basic Knowledge ◽  
Regulatory Role ◽  
Rna Molecules ◽  
Cell Compartments ◽  
Non Coding Rna ◽  
Related Mortality

Breast cancer is the most prevalent and incident female neoplasm worldwide. Although survival rates have considerably improved, it is still the leading cause of cancer-related mortality in women. MicroRNAs are small non-coding RNA molecules that regulate the posttranscriptional expression of a wide variety of genes. Although it is usually located in the cytoplasm, several studies have detected a regulatory role of microRNAs in other cell compartments such as the nucleus or mitochondrion, known as “mitomiRs”. MitomiRs are essential modulators of mitochondrion tasks and their abnormal expression has been linked to the aetiology of several human diseases related to mitochondrial dysfunction, including breast cancer. This review aims to examine basic knowledge of the role of mitomiRs in breast cancer and discusses their prospects as biomarkers or therapeutic targets.

scholarly journals USP1 Regulates TAZ Protein Stability Through Ubiquitin Modifications in Breast Cancer

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3090
Author(s):  
Ashley Mussell ◽  
He Shen ◽  
Yanmin Chen ◽  
Michalis Mastri ◽  
Kevin H. Eng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Protein Stability ◽  
Cancer Patients ◽  
Effector Proteins ◽  
Therapeutic Interventions ◽  
Hippo Signaling ◽  
Strong Positive Correlation ◽  
Breast Cancer Patients ◽  
Loss Of Function

The Hippo signaling pathway is an evolutionarily conserved pathway that was initially discovered in Drosophila melanogaster and was later found to have mammalian orthologues. The key effector proteins in this pathway, YAP/TAZ, are often dysregulated in cancer, leading to a high degree of cell proliferation, migration, metastasis and cancer stem cell populations. Due to these malignant phenotypes it is important to understand the regulation of YAP/TAZ at the protein level. Using an siRNA library screen of deubiquitinating enzymes (DUBs), we identified ubiquitin specific peptidase 1 (USP1) as a novel TAZ (WWTR1) regulator. We demonstrated that USP1 interacts with TAZ and increases TAZ protein stability. Conversely, loss of function of USP1 reduces TAZ protein levels through increased poly-ubiquitination, causing a decrease in cell proliferation and migration of breast cancer cells. Moreover, we showed a strong positive correlation between USP1 and TAZ in breast cancer patients. Our findings facilitate the attainment of better understanding of the crosstalk between these pathways and may lead to potential therapeutic interventions for breast cancer patients.

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