CD147 drives keloid formation by promoting fibroblast proliferation via the CENPF signaling pathway

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.

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Publication Details

Journal
iScience
Published
2026-10-17
DOI
https://doi.org/10.1016/j.isci.2026.117927
Primary Topic
Dermatologic Treatments and Research
Type
article
Field-Weighted Citation Impact
0.00

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article

CD147 drives keloid formation by promoting fibroblast proliferation via the CENPF signaling pathway

DU Hui-cong, Jian‐Sheng Diao, Md Atiqur Rahman, Maoguo Shu et al.
iScience
Dermatologic Treatments and Research
article

CD147 drives keloid formation by promoting fibroblast proliferation via the CENPF signaling pathway

DU Hui-cong, Jian‐Sheng Diao, Md Atiqur Rahman, Maoguo Shu, Zhuo Zhang, Jing Jia, Juan Wu, Xin-Nan Han
article en

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.

iScienceVol. 29(11)
First Affiliated Hospital of Xi'an Jiaotong University (CN), East West Medical College Hospital (BD)
National Natural Science Foundation of China, Natural Science Basic Research Program of Shaanxi Province
Good health and well-being
Openalex Percentile: Top 10%
Dermatologic Treatments and Research
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