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Updated: May 4, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Enhanced Expression of IL32 mRNA in Skeletal Muscles in the Context of Head and Neck Carcinomas
Imane Baïche1, Héla Hachicha1, Thierry Ragot1
1CNRS UMR 9018-METSY, Gustave Roussy and Université Paris-Saclay, Villejuif, France.
Background:
Cancer-related sarcopenia (CRS) is a significant complication of head and neck carcinoma (HNC), characterised by muscle degeneration and poor clinical outcomes. Although various dietary and therapeutic interventions have been explored, most of them remain empirical, and the molecular mechanisms underlying CRS are not yet fully understood.
Methods:
Transcription profiles of muscle fragments from 29 HNC patients and 8 control donors were analysed by bulk RNA sequencing (6/29 and 3/8) and/or RT-qPCR (29/29 and 5/8). In parallel, differentiating human myoblasts (AB1190) were subjected to indirect co-culture with two types of effector cells: HNC cells (FaDu) or control epithelial cells (NHEK). The contactless effects of effector cells on target myoblasts were investigated using cell imaging to assess muscular differentiation, RT-qPCR and Western blot to assess gene expression.
Results:
Bulk RNA sequencing identified 789 differentially expressed transcripts between HNC and control samples. Subsequent RT-qPCR analysis focused on IL32 and BIRC3 mRNAs (up-regulated in HNC samples) and ACE1 mRNA (down-regulated). Among male HNC patients, the IL32/ACE1 mRNA ratio was significantly elevated in CRS cases (p = 0.0001, effect size r = 0.57) and correlated with the severity of muscle atrophy (negative correlation with the Skeletal Muscle Index at a threshold of 10%: p = 0.093, r = -0.41). In contrast, no such trend was observed for the BIRC3/ACE1 ratio. Exposure of human myoblasts to HNC cells induced inhibition of myogenesis and strong up-regulation of IL32 mRNA and protein. In contrast, these effects were absent or much smaller under exposure to NHEK controls.
Conclusions:
IL32 is a potential biomarker for CRS in HNC patients. In addition, the HNC-myoblast co-cultivation model provides a promising in vitro system to study CRS mechanisms, potentially reducing the reliance on animal models.
Insights
Interleukin-32 (IL32) is identified as a key factor in cancer-related sarcopenia (CRS) for head and neck cancer (HNC) patients. This discovery offers a potential biomarker for CRS and an improved in vitro model for studying muscle degeneration.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Cancer-related sarcopenia (CRS) is a serious complication in head and neck carcinoma (HNC) patients, leading to muscle wasting and poor outcomes.
- Current understanding of CRS molecular mechanisms is limited, with many interventions being empirical.
Purpose of the Study:
- To investigate the molecular mechanisms underlying cancer-related sarcopenia in head and neck cancer.
- To identify potential biomarkers for CRS in HNC patients.
Main Methods:
- Bulk RNA sequencing and RT-qPCR were used to analyze muscle tissue from HNC patients and controls.
- In vitro co-culture systems with human myoblasts and HNC cells were employed to study cellular interactions.
- Cell imaging, RT-qPCR, and Western blot were used to assess gene expression and protein levels.
Main Results:
- Bulk RNA sequencing revealed 789 differentially expressed transcripts between HNC and control samples.
- The IL32/ACE1 mRNA ratio was significantly elevated in male HNC patients with CRS and correlated with muscle atrophy.
- In vitro, HNC cells induced myogenesis inhibition and IL32 upregulation in myoblasts, unlike control cells.
Conclusions:
- Interleukin-32 (IL32) is a potential biomarker for cancer-related sarcopenia in head and neck cancer patients.
- The HNC-myoblast co-cultivation model offers a valuable in vitro system for studying CRS mechanisms, potentially reducing animal model use.

