scholarly journals Role of myokines and osteokines in cancer cachexia

2021 ◽  
pp. 153537022110092
Author(s):  
Fabrizio Pin ◽  
Lynda F Bonewald ◽  
Andrea Bonetto
Keyword(s):  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Skeletal Muscle Atrophy ◽  
Lipid Mediator ◽  
Promising Strategy ◽  
Different Types ◽  
Ultimate Cause ◽  
Endocrine Factors ◽  
Shed Light

Cancer-induced muscle wasting, i.e. cachexia, is associated with different types of cancer such as pancreatic, colorectal, lung, liver, gastric and esophageal. Cachexia affects prognosis and survival in cancer, and it is estimated that it will be the ultimate cause of death for up to 30% of cancer patients. Musculoskeletal alterations are known hallmarks of cancer cachexia, with skeletal muscle atrophy and weakness as the most studied. Recent evidence has shed light on the presence of bone loss in cachectic patients, even in the absence of bone-metastatic disease. In particular, we and others have shown that muscle and bone communicate by exchanging paracrine and endocrine factors, known as myokines and osteokines. This review will focus on describing the role of the most studied myokines, such as myostatin, irisin, the muscle metabolite β-aminoisobutyric acid, BAIBA, and IL-6, and osteokines, including TGF-β, osteocalcin, sclerostin, RANKL, PTHrP, FGF23, and the lipid mediator, PGE2 during cancer-induced cachexia. The interplay of muscle and bone factors, together with tumor-derived soluble factors, characterizes a complex clinical scenario in which musculoskeletal alterations are amongst the most debilitating features. Understanding and targeting the “secretome” of cachectic patients will likely represent a promising strategy to preserve bone and muscle during cancer cachexia thereby enhancing recovery.

scholarly journals Exercise as an anti-inflammatory therapy for cancer cachexia: a focus on interleukin-6 regulation

2020 ◽  
Vol 318 (2) ◽  
pp. R296-R310 ◽  
Author(s):  
Hélène N. Daou
Keyword(s):  
Skeletal Muscle ◽  
Systemic Inflammation ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Skeletal Muscle Atrophy ◽  
Ampk Signaling ◽  
Skeletal Muscle Wasting ◽  
Skeletal Muscle Loss ◽  
Anti Inflammatory ◽  
Tumor Growth And Metastasis

Cancer cachexia is a complicated disorder of extreme, progressive skeletal muscle wasting. It is directed by metabolic alterations and systemic inflammation dysregulation. Numerous studies have demonstrated that increased systemic inflammation promotes this type of cachexia and have suggested that cytokines are implicated in the skeletal muscle loss. Exercise is firmly established as an anti-inflammatory therapy that can attenuate or even reverse the process of muscle wasting in cancer cachexia. The interleukin IL-6 is generally considered to be a key player in the development of the microenvironment of malignancy; it promotes tumor growth and metastasis by acting as a bridge between chronic inflammation and cancerous tissue and it also induces skeletal muscle atrophy and protein breakdown. Paradoxically, a beneficial role for IL-6 has also been identified recently, and that is its status as a “founding member” of the myokine class of proteins. Skeletal muscle is an important source of circulating IL-6 in people who participate in exercise training. IL-6 acts as an anti-inflammatory myokine by inhibiting TNFα and improving glucose uptake through the stimulation of AMPK signaling. This review discusses the action of IL-6 in skeletal muscle tissue dysfunction and the role of IL-6 as an “exercise factor” that modulates the immune system. This review also sheds light on the main considerations related to the treatment of muscle wasting in cancer cachexia.

The role of cytokines in muscle wasting: Its relation with cancer cachexia

1992 ◽  
Vol 12 (6) ◽  
pp. 637-652 ◽  
Author(s):  
Josep M. Argilés ◽  
Cèlia Garcia-Martínez ◽  
Maria Llovera ◽  
Francisco J. López-Soriano
Keyword(s):  
Cancer Cachexia ◽  
Muscle Wasting

scholarly journals Transcriptomic analysis of the development of skeletal muscle atrophy in cancer-cachexia in tumor-bearing mice

2018 ◽  
Vol 50 (12) ◽  
pp. 1071-1082 ◽  
Author(s):  
Thomas A. Blackwell ◽  
Igor Cervenka ◽  
Bhuwan Khatri ◽  
Jacob L. Brown ◽  
Megan E. Rosa-Caldwell ◽  
...  
Keyword(s):  
Time Course ◽  
Gastrocnemius Muscle ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Global Gene Expression ◽  
Skeletal Muscle Atrophy ◽  
Cytoskeletal Structure ◽  
Protein Ubiquitination ◽  
Global Gene Expression Analysis ◽  
Cellular Pathways

Cancer-cachexia (CC) is a wasting condition directly responsible for 20–40% of cancer-related deaths. The mechanisms controlling development of CC-induced muscle wasting are not fully elucidated. Most investigations focus on the postcachectic state and do not examine progression of the condition. We recently demonstrated mitochondrial degenerations precede muscle wasting in time course progression of CC. However, the extent of muscle perturbations before wasting in CC is unknown. Therefore, we performed global gene expression analysis in CC-induced muscle wasting to enhance understanding of intramuscular perturbations across the development of CC. Lewis lung carcinoma (LLC) was injected into the hind-flank of C57BL6/J mice at 8 wk of age with tumor allowed to develop for 1, 2, 3, or 4 wk and compared with PBS-injected control. Muscle wasting was evident at 4 wk LLC. RNA sequencing of gastrocnemius muscle samples showed widespread alterations in LLC compared with PBS animals with largest differences seen in 4 wk LLC, suggesting extensive transcriptomic alterations concurrent to muscle wasting. Commonly altered pathways included: mitochondrial dysfunction and protein ubiquitination, along with other less studied processes in this condition regulating transcription/translation and cytoskeletal structure. Current findings present novel evidence of transcriptomic shifts and altered cellular pathways in CC-induced muscle wasting.

scholarly journals Comics in the Arab world. Birth and spread of a new literary genre

2020 ◽  
Vol 31 ◽  
pp. 117-126
Author(s):  
Emanuela De Blasio
Keyword(s):  
Social Networks ◽  
Arab World ◽  
Arab Countries ◽  
The Internet ◽  
Literary Genre ◽  
The West ◽  
Arab Culture ◽  
Different Types ◽  
Shed Light

The research focuses on the birth and development of the comics, a new literary genre in the Arab world. The paper takes into account the dynamics of the advent of comics in the first Arab countries until to our days when comics began to appeal to an adult audience, sometimes taking inspiration from material from the West, sometimes referring to traditional elements of Arab culture. With the advent of the Arab revolutions, this genre has become more widespread and has also been used by artists to express dissent and criticism. Following the fall of dictatorial regimes in some Arab countries, the power of censorship has diminished; this has allowed the proliferation of different types of comics, also thanks to the fundamental role of social networks and the Internet. Through the examination of comics in the Arab world it is possible to shed light on a new literary genre and it is possible to trace the lines of the evolution of its themes and language.

scholarly journals Nutraceuticals and Exercise against Muscle Wasting during Cancer Cachexia

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2536
Author(s):  
Giorgio Aquila ◽  
Andrea David Re Cecconi ◽  
Jeffrey J. Brault ◽  
Oscar Corli ◽  
Rosanna Piccirillo
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscles ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Premature Death ◽  
Preclinical Studies ◽  
Current State ◽  
Causal Therapy ◽  
And Oxidative Stress

Cancer cachexia (CC) is a debilitating multifactorial syndrome, involving progressive deterioration and functional impairment of skeletal muscles. It affects about 80% of patients with advanced cancer and causes premature death. No causal therapy is available against CC. In the last few decades, our understanding of the mechanisms contributing to muscle wasting during cancer has markedly increased. Both inflammation and oxidative stress (OS) alter anabolic and catabolic signaling pathways mostly culminating with muscle depletion. Several preclinical studies have emphasized the beneficial roles of several classes of nutraceuticals and modes of physical exercise, but their efficacy in CC patients remains scant. The route of nutraceutical administration is critical to increase its bioavailability and achieve the desired anti-cachexia effects. Accumulating evidence suggests that a single therapy may not be enough, and a bimodal intervention (nutraceuticals plus exercise) may be a more effective treatment for CC. This review focuses on the current state of the field on the role of inflammation and OS in the pathogenesis of muscle atrophy during CC, and how nutraceuticals and physical activity may act synergistically to limit muscle wasting and dysfunction.

scholarly journals MicroRNAs in Skeletal Muscle and Hints on Their Potential Role in Muscle Wasting During Cancer Cachexia

2020 ◽  
Vol 10 ◽  
Author(s):  
Gioacchino P. Marceca ◽  
Giovanni Nigita ◽  
Federica Calore ◽  
Carlo M. Croce
Keyword(s):  
Skeletal Muscle ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Phenotypic Alteration ◽  
Specific Tumor ◽  
Non Coding Rnas

Cancer-associated cachexia is a heterogeneous, multifactorial syndrome characterized by systemic inflammation, unintentional weight loss, and profound alteration in body composition. The main feature of cancer cachexia is represented by the loss of skeletal muscle tissue, which may or may not be accompanied by significant adipose tissue wasting. Such phenotypic alteration occurs as the result of concomitant increased myofibril breakdown and reduced muscle protein synthesis, actively contributing to fatigue, worsening of quality of life, and refractoriness to chemotherapy. According to the classical view, this condition is primarily triggered by interactions between specific tumor-induced pro-inflammatory cytokines and their cognate receptors expressed on the myocyte membrane. This causes a shift in gene expression of muscle cells, eventually leading to a pronounced catabolic condition and cell death. More recent studies, however, have shown the involvement of regulatory non-coding RNAs in the outbreak of cancer cachexia. In particular, the role exerted by microRNAs is being widely addressed, and several mechanistic studies are in progress. In this review, we discuss the most recent findings concerning the role of microRNAs in triggering or exacerbating muscle wasting in cancer cachexia, while mentioning about possible roles played by long non-coding RNAs and ADAR-mediated miRNA modifications.

scholarly journals Role of Exosomal MicroRNAs and myomiRs in the Development of Cancer Cachexia-Associated Muscle Wasting

2018 ◽  
Vol 4 ◽  
Author(s):  
Rodolfo Marinho ◽  
Paulo S. M. Alcântara ◽  
José P. Ottoch ◽  
Marilia Seelaender
Keyword(s):  
Cancer Cachexia ◽  
Muscle Wasting

Resveratrol does not ameliorate muscle wasting in different types of cancer cachexia models

2007 ◽  
Vol 26 (2) ◽  
pp. 239-244 ◽  
Author(s):  
Sílvia Busquets ◽  
Gemma Fuster ◽  
Elisabet Ametller ◽  
Mireia Olivan ◽  
Maite Figueras ◽  
...  
Keyword(s):  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Different Types

Targeting NUPR1 for Cancer Treatment: A Risky Endeavor

2020 ◽  
Vol 20 (10) ◽  
pp. 768-778
Author(s):  
Salma M.A. Mansour ◽  
Sahar A. Ali ◽  
Shaira Nofal ◽  
Sameh H. Soror
Keyword(s):  
Transcription Factor ◽  
Cancer Treatment ◽  
Complex Network ◽  
Mechanism Of Action ◽  
Molecular Targets ◽  
Novel Therapies ◽  
Different Types ◽  
Shed Light

NUPR1 is a transcription factor that has attracted great attention because of its various roles in cancer. Several studies were carried out to determine its molecular targets and mechanism of action to develop novel therapies against cancer. Here, we shed light on the role of NUPR1 in different types of cancer. NUPR1 regulates a complex network of pathways that may be affected by its silencing, which can cause varying effects. Its role in some types of cancer has been reported but remains incompletely understood, whereas its roles in other types of cancers have not been reported yet. Therefore, targeting NUPR1 for cancer treatment remains challenging and risky.

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