iScience· 2026Q1
CD147 drives keloid formation by promoting fibroblast proliferation via the CENPF signaling pathway
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- Q1SCImago
- 2026year
Short summary
CD147 is upregulated in keloid fibroblasts (KFs) and drives their hyperproliferation by regulating the cell cycle via the centromere protein F (CENPF) pathway, with CENPF knockdown attenuating CD147's effects.
AI-generated from the title and abstract; the full text is not read.
Key points
- CD147 is upregulated in keloid fibroblasts (KFs) and promotes their pathological proliferation.
- CD147 regulates the KF cell cycle, and its inhibition leads to downregulation of centromere protein F (CENPF).
- Knockdown of CENPF attenuates the proliferation-promoting effects of CD147 in KFs.
- The CD147-CENPF signaling pathway is implicated in keloid pathogenesis.
AI-generated from the title and abstract; the full text is not read.
Abstract
Keloids are benign dermal tumors, and keloid fibroblasts (KFs) play a critical role in their formation through hyperproliferation. However, the mechanism underlying this excessive fibroblast growth in keloids remains elusive. Here, we demonstrate that CD147 is upregulated in KFs and promotes their pathological activities, while its inhibition reverses these abnormalities. RNA sequencing (RNA-seq) analysis revealed that CD147 played an important regulatory role in controlling the cell cycle of KFs, and centromere protein F (CENPF) expression was substantially downregulated following CD147 inhibition. Furthermore, CENPF knockdown attenuated the proliferation-inducing effects of CD147 in KFs, potentially promoting cell apoptosis via the p53 signaling pathway. These findings uncover the CD147-CENPF signaling pathway in keloid pathogenesis, suggesting targeting this pathway as a promising therapeutic strategy.
The authors' abstract, as published at the source. iScience, 2026 · DOI ↗
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Field: Dermatology
DermatologyMedicine