IFIT2‐depleted metastatic oral squamous cell carcinoma cells induce muscle atrophy and cancer cachexia in mice

Background Interferon‐induced protein with tetratricopeptide repeat 2 (IFIT2) is a reported metastasis suppressor in oral squamous cell carcinoma (OSCC). Metastases and cachexia may coexist. The effect of cancer metastasis on cancer cachexia is largely unknown. We aimed to address this gap in knowle...

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Veröffentlicht in:Journal of cachexia, sarcopenia and muscle sarcopenia and muscle, 2022-04, Vol.13 (2), p.1314-1328
Hauptverfasser: Lai, Kuo‐Chu, Hong, Zi‐Xuan, Hsieh, Jyh‐Gang, Lee, Hui‐Ju, Yang, Muh‐Hwa, Hsieh, Chia‐Husu, Yang, Cheng‐Han, Chen, Yan‐Ru
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Sprache:eng
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Zusammenfassung:Background Interferon‐induced protein with tetratricopeptide repeat 2 (IFIT2) is a reported metastasis suppressor in oral squamous cell carcinoma (OSCC). Metastases and cachexia may coexist. The effect of cancer metastasis on cancer cachexia is largely unknown. We aimed to address this gap in knowledge by characterizing the cachectic phenotype of an IFIT2‐depleted metastatic OSCC mouse model. Methods Genetically engineered and xenograft tumour models were used to explore the effect of IFIT2‐depleted metastatic OSCC on cancer cachexia. Muscle and organ weight changes, tumour burden, inflammatory cytokine profiles, body composition, food intake, serum albumin and C‐reactive protein (CRP) levels, and survival were assessed. The activation of the IL6/p38 pathway in atrophied muscle was measured. Results IFIT2‐depleted metastatic tumours caused marked body weight loss (−18.2% vs. initial body weight, P 
ISSN:2190-5991
2190-6009
DOI:10.1002/jcsm.12943