RIPOR2 promotes multinucleation of melanoma cells downstream of the RAS/ERK oncogenic pathway
Wilmerding A., Richard A., Macagno N., Hirsinger E., Gharsalli T., Bellenger L.
Animal Study, published in iScience (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- 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
- Animal Study
- Journal
- iScience (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 42100747
- PMCID
- PMC13145898
- DOI
- 10.1016/j.isci.2026.115734
Abstract (original English)
Multinucleation in cancer has been shown to promote aneuploidy, which correlates with tumor aggressiveness. This is particularly true for melanoma, a cancer caused by excessive proliferation of melanocytes, whose RAS/ERK pathway is overactivated. Using single-nucleus RNA sequencing after overactivation of the RAS/ERK pathway in the chicken embryo as an in vivo model, we discovered that RIPOR2 is a positive transcriptional target of this pathway, including in melanocyte precursors. Similar transcriptional control of RIPOR2 by RAS/ERK is conserved in human melanoma cells. RIPOR2 emerged as an attractive target because it encodes an atypical RHOA inhibitory protein involved in the development of physiologically multinucleated cell types. We found that RIPOR2 is ectopically expressed in human melanoma and functionally promotes multinucleation in both an animal model and human tumor-derived cells, including melanoma cell lines. Our results suggest that RIPOR2 expression, downstream of RAS/ERK overactivation, may contribute to melanocyte transformation by promoting multinucleation.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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