ArticleJournal of cachexia, sarcopenia and muscle2025
SIRT6 Ameliorates Cancer Cachexia-Associated Adipose Wasting by Suppressing TNFR2 Signalling in Mice.
Article in Journal of cachexia, sarcopenia and muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The prognostic value of CT-quantified visceral and subcutaneous fat areas in sepsis.World journal of emergency medicine · 2026Article
- From mechanisms to management: a comprehensive review of sarcopenia in gastric cancer.Frontiers in nutrition · 2026Review
- SIRT6 in Cancer: Mechanistic Insights into Its Dual Roles in Cancer Biology and Implications for Precision Therapeutic Development.Biomolecules · 2025Review
- The Functions and Regulatory Mechanisms of Histone Modifications in Skeletal Muscle Development and Disease.International journal of molecular sciences · 2025Review
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13 authors.
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Abstract
backgroundCachexia is a wasting syndrome associated with imbalanced energy metabolism and loss of adipose and muscle tissues and contributes to morbidity and mortality in ageing as well as in patients with severe chronic diseases, including cancer. At present, there are no treatments addressing cachexia that have reached validation to be used in the clinic. In this study, we investigate the protective role of SIRT6, an important regulator of energy homeostasis and health preservation, against Lewis lung carcinoma (LLC)-induced cachexia.
methodsSIRT6 levels of serum from gastric cancer patients (n = 22, 65.27 ± 12.50 years old, 40.9% females) and healthy controls (n = 22, 63.50 ± 10.77 years old, 45.4% females) were measured to evaluate the correlation between circulating SIRT6 levels and cancer cachexia development. Ten-week-old SIRT6 transgenic (TG) and wild type (WT) male mice injected with LLC cells (1.5 × 10
resultsSIRT6 concentrations were significantly higher in non-cachectic cancer patients (3.41 ± 0.30 ng/mL) compared to cachectic cancer patients (3.20 ± 0.23 ng/mL, p < 0.01), suggesting the negative correlation between SIRT6 level and cachexia in patients with cancer. SIRT6 overexpression significantly ameliorated tumour-induced wasting and energy expenditure in white adipose tissues (eWAT mass loss: 66% in WT vs. 32% in TG; iWAT mass loss: 69% in WT vs. 40% in TG) through suppression of browning and lipolysis. In LLC-induced cachexia, tumour necrosis factor-α receptor 2 (TNFR2) mediated the inhibition of SIRT6 on lipolytic signalling, because the difference in lipolysis between the WT and SIRT6 knockout group was almost eliminated by TNFR2 neutralizing antibody. Increased serum TNFR2 concentration was found in cachectic cancer patients (690.41 pg/mL in non-cachectic vs. 1166.98 pg/mL in cachectic patients, p < 0.05). A selective SIRT6 pharmaceutical activator, MDL800, could completely reverse LLC-induced lipolysis in adipocytes.
conclusionWe found an unexpected beneficial function of SIRT6 in cancer cachexia, demonstrating that increased SIRT6 expression or activity is capable of protecting the host against cachexia-associated tissue wasting, providing a concept of future therapies for cachexia.
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