ArticleAutophagy2025
TRIM16 mediates secretory autophagy in head and neck cancer-associated fibroblasts.
Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Autophagy determines the fate of immune cells by regulating metabolic remodeling and PANoptosis (Review).International journal of molecular medicine · 2026Review
- Secretory autophagy mediates SLC16A3/MCT4-dependent lactate secretion to drive metastatic progression in triple-negative breast cancer.Autophagy · 2026Article
- Targeting VAMPs in Aging-Related Diseases: From Mechanisms to Pharmacotherapy.Pharmaceutical research · 2026Review
- Oxidative stress induced by DMSA-IONPs impairs breast cancer cell migration and paracrine cell communication.Journal of nanobiotechnology · 2026Article
- Mechanisms, strategies, and clinical application progress of subcutaneous transplantation angiogenesis.Frontiers in bioengineering and biotechnology · 2025Review
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Improving treatment options for head and neck squamous cell carcinoma (HNSCC) requires a deeper understanding of the tumor microenvironment, particularly cancer-associated fibroblasts (CAFs). We previously reported that HNSCC-derived FGF2/bFGF (fibroblast growth factor 2) triggers cytokine release from CAFs via secretory autophagy. Here, using transmission electron microscopy, live-cell imaging, and immunofluorescence, we show that CAF autophagosomes transport cargo, including IL6, to the plasma membrane for secretion. Autophagy in CAFs is constitutive and independent of STAT3, MAPK1/ERK2-MAPK3/ERK1 and phosphoinositide 3-kinase (PI3K) signaling. Despite the significant role of secretory autophagy in CAFs, its molecular machinery has remained elusive. Using both a literature based, and an unbiased approach, we studied the molecular machinery involved in autophagosome trafficking in CAFs. We identified TRIM16, a protein previously reported to traffic to autophagosomes, upregulated in CAFs compared to normal oral fibroblasts. Immunohistochemistry of patient HNSCC stroma revealed co-expression of TRIM16 and LC3B, linking TRIM16 to autophagosome function. An unbiased proteomics profiling of immunoprecipitated LC3B
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.