ArticleInternational wound journal2023
FBXL6 is dysregulated in keloids and promotes keloid fibroblast growth by inducing c-Myc expression.
Article in International wound journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Exosomes Derived from Non-small Cell Lung Cancer Cells Transfer LINC00467 to Induce the Proliferation of Cancer-associated Fibroblasts.Cell biochemistry and biophysics · 2026Article
- Epidemiology of keloids among university students in Uganda.Dermatology reports · 2026Article
- Adipose Stem Cell-Derived Apoptotic Vesicles Attenuate Hypertrophic Scarring by Targeting the CDC20/WNT Signaling Pathway.Biomedicines · 2026Article
- Deoxyshikonin inhibits growth and induces apoptosis of hypertrophic scar-derived fibroblasts by downregulating FBXO expression through autophagy.Scientific reports · 2026Article
- Mechanism of β‑sitosterol in treating keloids: Network pharmacology, molecular docking and experimental verification.Molecular medicine reports · 2025Article
- ALKBH5 Inhibits YTHDF2-m6A-Mediated Degradation of RCN1 mRNA to Promote Keloid Formation by Activating IRE1α-XBP1-Mediated ER Stress.Journal of cosmetic dermatology · 2025Article
- MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024Review
- The deubiquitinating enzyme USP37 promotes keloid fibroblasts proliferation and collagen production by regulating the c-Myc expression.International wound journal · 2023Article
- FBXL6 is dysregulated in keloids and promotes keloid fibroblast growth by inducing c-Myc expression.International wound journal · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-MYC-mediated keloid fibroblasts proliferation and collagen deposit may contribute to the development of keloids. F-box and leucine-rich repeat protein 6 (FBXL6) is reported to be involved in tumour progression, while the role of FBXL6 in keloid fibroblasts is not deciphered. Normal control skins, hypertrophic scars and keloid tissues were collected and prepared for FBXL6 detection. FBXL6 short hairpin RNAs (shRNAs) or FBXL6 over-expression plasmids were transfected into keloid fibroblasts, and then c-MYC plasmids were further transfected. Cell viability was assayed with a Cell-Counting Kit-8 kit. The relative expression of FBXL6, Cyclin A1, Cyclin D2, Cyclin E1 and Collagen I was detected with real-time PCR and Western blot. Elevated FBXL6 expression could be observed in keloid tissues and hypertrophic scars. FBXL6 shRNAs transfection could inhibit the viability of keloid fibroblasts with diminished c-MYC expression and down-regulated Cyclin A1, Cyclin D2, Cyclin E1 and Collagen I expression. At the same time, overexpressed FBXL6 could promote the proliferation of keloid fibroblasts. Overexpression of c-MYC could promote the proliferation of keloid fibroblasts reduced by FBXL6 shRNAs with up-regulated Cyclin A1 and Collagen I expression. FBXL6 could promote the growth of keloid fibroblasts by inducing c-MYC expression, which could be targeted in keloids treatment.
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Registered trials
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