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

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.

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BibTeX RIS

BibTeX

@article{diao2026cd147,
  title = {{CD147 drives keloid formation by promoting fibroblast proliferation via the CENPF signaling pathway}},
  author = {Jian-Sheng Diao and Xin-Nan Han and Hui-Cong Du and Juan Wu and Jing Jia and Zhuo Zhang and Md Atiqur Rahman and Mao-Guo Shu},
  journal = {iScience},
  year = {2026},
  month = oct,
  doi = {10.1016/j.isci.2026.117927},
  url = {https://www.cell.com/iscience/fulltext/S2589-0042(26)03310-9},
  note = {CC BY-NC-ND 4.0},
}

RIS

TY  - JOUR
TI  - CD147 drives keloid formation by promoting fibroblast proliferation via the CENPF signaling pathway
AU  - Jian-Sheng Diao
AU  - Xin-Nan Han
AU  - Hui-Cong Du
AU  - Juan Wu
AU  - Jing Jia
AU  - Zhuo Zhang
AU  - Md Atiqur Rahman
AU  - Mao-Guo Shu
PY  - 2026
DA  - 2026/10/17
JO  - iScience
DO  - 10.1016/j.isci.2026.117927
UR  - https://www.cell.com/iscience/fulltext/S2589-0042(26)03310-9
AB  - 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.
SN  - 2589-0042
ER  -

Abstract

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