ArticleCell death & disease2021
HOXA5 counteracts the function of pathological scar-derived fibroblasts by partially activating p53 signaling.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Identification and Verification of SLC6A15 Involved in Keloid via Bioinformatics Analysis and Machine Learning.Biochemical genetics · 2026Article
- Fibroblast mechanoperception instructs pulmonary developmental and pattern specification gene expression programs.PLoS genetics · 2025Article
- HOX and MEINOX in cellular plasticity, fibrosis, and cancer.World journal of stem cells · 2025Review
- Article
- Bacterial colonization contributes to pathological scar formation via the regulation of inflammatory response.Journal of translational medicine · 2025Article
- FOXO4-DRI induces keloid senescent fibroblast apoptosis by promoting nuclear exclusion of upregulated p53-serine 15 phosphorylation.Communications biology · 2025Article
- HOXA5-mediated spatial remodeling of tumor-immune interfaces across cancers promotes AML pathogenesis.Frontiers in immunology · 2025Article
- Efficient protocol for isolating human fibroblast from primary skin cell cultures: application to keloid, hypertrophic scar, and normal skin biopsies.Biology methods & protocols · 2024Article
- MiR-29b Downregulation by p53/Sp1 Complex Plays a Critical Role in Bleb Scar Formation After Glaucoma Filtration Surgery.Translational vision science & technology · 2023Article
- The circular RNANeural regeneration research · 2023Article
- Progress in the clinical treatment of keloids.Frontiers in medicine · 2023Review
- MicroRNA-182-5p Inhibits Hypertrophic Scar Formation by Inhibiting the Proliferation and Migration of Fibroblasts via SMAD4 Pathway.Clinical, cosmetic and investigational dermatology · 2023Article
- LncRNA FPASL suppresses fibroblast proliferation through its DNA methylation via DNMT3b in hypertrophic scar.Acta biochimica et biophysica Sinica · 2022Article
- A novel lncRNA FPASL regulates fibroblast proliferation via the PI3K/AKT and MAPK signaling pathways in hypertrophic scar.Acta biochimica et biophysica Sinica · 2022Article
- Hoxa5 Inhibits the Proliferation and Induces Adipogenic Differentiation of Subcutaneous Preadipocytes in Goats.Animals : an open access journal from MDPI · 2022Article
- Transition of autophagy and apoptosis in fibroblasts depends on dominant expression of HIF-1α or p53.Journal of Zhejiang University. Science. B · 2022Article
- Homeobox Genes in Cancers: From Carcinogenesis to Recent Therapeutic Intervention.Frontiers in oncology · 2021Review
- Circ_0057452 functions as a ceRNA in hypertrophic scar fibroblast proliferation and VEGF expression by regulating TGF-β2 expression and adsorbing miR-145-5p.American journal of translational research · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inactivation of p53 can lead to the formation of pathological scars, including hypertrophic scars and keloids. HOXA5 has been reported to be a critical transcription factor in the p53 pathway in cancers. However, whether HOXA5 also plays a role in pathological scar progression through activating p53 signaling remains unknown. In this study, we first demonstrated that HOXA5 overexpression in hypertrophic scar-or keloids-derived fibroblasts decreased cell proliferation, migration and collagen synthesis, whereas increased cell apoptosis. Furthermore, the results of luciferase activity assays and ChIP PCR assays indicated that HOXA5 transactivated p53 by binding to the ATTA-rich core motif in the p53 promoter. HOXA5 also increased the levels of p21 and Mdm2, which are downstream targets of p53. Interestingly, silencing p53 in these pathological scar-derived fibroblasts partially attenuated HOXA5-mediated growth inhibition effect and HOXA5-induced apoptosis. In addition, 9-cis-retinoic acid augmented the expression of HOXA5 and promoted the effects of HOXA5 on pathological scar-derived fibroblasts, and these effects could be suppressed by HOXA5 knockdown. Thus, our study reveals a role of HOXA5 in mediating the cellular processes of pathological scar-derived fibroblasts by transcriptionally activating the p53 signaling pathway, and 9-cis-retinoic acid may be a potential therapy for pathological scars.
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