Expression of TRAF6 and ubiquitin mRNA in skeletal muscle of gastric cancer patients

Sun, Yuanshui; Ye, Zai-yuan; Qian, Zhenyuan; Xu, Xiaodong; Hu, Jian

doi:10.1186/1756-9966-31-81

Cited by 39 publications

(25 citation statements)

References 12 publications

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“…The ubiquitin-proteasome system (UPS) is the major proteolytic machinery systematically activated in cachexia, and only proteasome inhibitors prevent increased proteolysis [12]. Sun et al [13] investigated the TRAF-6 expression in patients with gastric cancer. They found that TRAF-6 was significantly up-regulated in the muscles involved in gastric cancer compared with the control muscles, and an overexpression of TRAF-6 in the muscles of gastric cancer was associated with TNM stage, level of serum albumin, and percent of weight loss.…”

Section: Discussionmentioning

confidence: 99%

The prognostic role of inflammation and hormones in patients with metastatic cancer with cachexia

et al. 2015

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We wanted to investigate the possible etiologic factors of cachexia. Forty-six patients diagnosed with cancer cachexia and 34 healthy controls were included in the study. Serum total testosterone, free testosterone, interleukin 1 (IL) alpha and beta, IL6, tumor necrosis factor (TNF) alpha, orexin, galanin, neuropeptide Y, tumor necrosis factor-like weak inducer of apoptosis and tumor necrosis factor receptor-associated factor 6, and C-reactive protein (CRP) levels were investigated. There were 36 male and 10 female patients in the cachexia group, and 24 male and 10 female patients in the control group. Median overall survival (OS) of the cachexia group after the diagnosis of cachexia was 8 (1-25) months. There were statistically significant relationships between OS and BMI, serum CRP, TRAF-6, albumin, and LDH levels in the cachexia group. In addition to cachexia, serum CRP, testosterone, and TNF alpha levels were statistically significantly correlated with OS in refractory cachexia. TRAF-6 levels was significantly correlated with type of cancer (P = 0.02). Although cachexia presents with a multifactorial ethio-pathogenesis, few of them affect the OS. Our novel results were that serum CRP, albumin, LDH, and TRAF-6 levels have a higher association with OS in patients with cancer cachexia compared to the many other parameters. An ongoing cachexia also called refractory cachexia is a recent definition. This end-stage term of cancer duration may be predicted by decreasing serum testosterone and increasing serum TNF alpha levels, as well as serum CRP levels.

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Section: Discussionmentioning

confidence: 99%

The prognostic role of inflammation and hormones in patients with metastatic cancer with cachexia

et al. 2015

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“…The role of TRAF6 in animal models of cancer cachexia was recently confirmed in a clinical study. Both TRAF6 and ubiquitin were found to be significantly upregulated in muscle of gastric cancer patients compared with muscles from patients with benign diseases [28]. Thus, TRAF6 has become an important therapeutic target for treating cancer cachexia.…”

Section: Cancer Cachexiamentioning

confidence: 99%

Cytokine Signaling in Skeletal Muscle Wasting

Zhou

Liu

Liang

et al. 2016

Trends in Endocrinology & Metabolism

144

104

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“…Another factor affecting skeletal muscle and upregulated during atrophy is TRAF6 (TNFα receptor adapter protein), which is also overexpressed in muscle from gastric cancer patients. 52, 53 Its inhibition has been shown to prevent skeletal muscle wasting induced by cachexia in experimental models. 53 …”

Section: Introductionmentioning

confidence: 99%

Understanding cachexia as a cancer metabolism syndrome

2016

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Metabolic reprogramming occurs in tumors to foster cancer cell proliferation, survival and metastasis, but as well at a systemic level affecting the whole organism, eventually leading to cancer cachexia. Indeed, as cancer cells rely on external sources of nitrogen and carbon skeleton to grow, systemic metabolic deregulation promoting tissue wasting and metabolites mobilization ultimately supports tumor growth. Cachectic patients experience a wide range of symptoms affecting several organ functions such as muscle, liver, brain, immune system and heart, collectively decreasing patients' quality of life and worsening their prognosis. Moreover, cachexia is estimated to be the direct cause of at least 20% of cancer deaths. The main aspect of cachexia syndrome is the unstoppable skeletal muscle and fat storage wasting, even with an adequate caloric intake, resulting in nutrient mobilization – both directly as lipid and amino acids and indirectly as glucose derived from the exploitation of liver gluconeogenesis – that reaches the tumor through the bloodstream. From a metabolic standpoint, cachectic host develops a wide range of dysfunctions, from increased insulin and IGF-1 resistance to induction of mitochondrial uncoupling proteins and fat tissue browning resulting in an increased energy expenditure and heat generation, even at rest. For a long time, cachexia has been merely considered an epiphenomenon of end-stage tumors. However, in specific tumor types, such as pancreatic cancers, it is now clear that patients present markers of tissue wasting at a stage in which tumor is not yet clinically detectable, and that host amino acid supply is required for tumor growth. Indeed, tumor cells actively promote tissue wasting by secreting specific factors such as parathyroid hormone-related protein and micro RNAs. Understanding the molecular and metabolic mediators of cachexia will not only advance therapeutic approaches against cancer, but also improve patients' quality of life.

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Expression of TRAF6 and ubiquitin mRNA in skeletal muscle of gastric cancer patients

Cited by 39 publications

References 12 publications

The prognostic role of inflammation and hormones in patients with metastatic cancer with cachexia

The prognostic role of inflammation and hormones in patients with metastatic cancer with cachexia

Cytokine Signaling in Skeletal Muscle Wasting

Understanding cachexia as a cancer metabolism syndrome

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