Adipocytes promote cancer stemness properties in oral squamous cell carcinoma through C3/C3AR axis and sphingolipid metabolism.
Qin TX., Zhu YY., Ng WH., Ng SK., Chek MF., Tang KD.
Prospective Study, published in Cancer Lett (2025) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Cancer Lett (2025)
- Country
- Ireland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40482908
- DOI
- 10.1016/j.canlet.2025.217848
Abstract (original English)
There is convincing evidence that being overweight or having obesity is associated with an increased risk of developing oral squamous cell carcinoma (OSCC). Despite OSCC frequently spread to the cervical lymph nodes, where adipose tissue is the predominant tissue within the microenvironment, it is still largely unknown whether adipocytes could contribute to the formation of oral cancer stem cells (CSCs) niche during the oral carcinogenesis. Here, we report that adipocytes promote the CSCs phenotype of OSCC cells through the activation of complement C3 (C3). Subsequent clinical data analysis revealed that the elevated levels of C3 and its receptor C3AR are associated with aggressive features and shorter survival in human OSCC patients. Furthermore, C3 exists as an autocrine factor and through C3AR interaction regulates OSCC stemness and properties such as cell proliferation, migration and invasion. On the other hand, C3 and C3AR were found to be highly abundant in adipocytes upon co-cultured with OSCC cells, demonstrating its paracrine effect on adipocyte-CSCs interaction, which in turn promotes CSC properties and supports oral carcinogenesis. Intriguingly, the inhibition of functional C3/C3AR axis by sphingosine, a bioactive sphingolipid metabolite, resulted in the suppression of OSCC cells growth and adipocyte-promoted oral CSC self-renewal. In conclusion, our findings provide
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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