ArticleInternational journal of molecular medicine2019
CUDC‑907 reverses pathological phenotype of keloid fibroblasts in vitro and in vivo via dual inhibition of PI3K/Akt/mTOR signaling and HDAC2.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- CUDC-907 attenuates pulmonary fibrosis by reversing HDAC1-mediated SMAD4 deacetylation at lysine 45.Biology direct · 2026Article
- Histone modifications in skin fibrosis: linking immune dysregulation, metabolic reprogramming, and persistent fibrotic remodeling.Frontiers in immunology · 2026Review
- Hypertrophic Scarring and Keloids: Epidemiology, Molecular Pathogenesis, and Therapeutic Interventions.MedComm · 2025Review
- Piezoelectric nanofilms fabricated by coaxial electrospun polycaprolactone/Barium titanate promote Achilles tendon regeneration by reducing IL-17A/NF-κB-mediated inflammation.Bioactive materials · 2025Article
- NUCKS1 promotes invasion and metastasis of colorectal cancer by stabilizing HDAC2 and activating AKT.Oncogenesis · 2025Article
- The PI3K/AKT/mTOR pathway in scar remodeling and keloid formation: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- The regulatory role of immune microenvironment-related cells and pathways in the pathogenesis of keloids.Frontiers in immunology · 2025Review
- Keloids as a Spectrum of Auto-Inflammatory Fibrotic Disorders: Beyond the Conventional Wound-Healing Paradigm.Clinical, cosmetic and investigational dermatology · 2025Review
- Emerging biomedical technologies for scarless wound healing.Bioactive materials · 2024Review
- Adipose stem cell exosomes promote mitochondrial autophagy through the PI3K/AKT/mTOR pathway to alleviate keloids.Stem cell research & therapy · 2024Article
- Comprehensive Insights into Keloid Pathogenesis and Advanced Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Diagnosis and management in Rubinstein-Taybi syndrome: first international consensus statement.Journal of medical genetics · 2024Review
- Future Directions About Keloid Scars Based on Pathogenesis and Therapies.Clinical, cosmetic and investigational dermatology · 2024Review
- Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023Review
- Mechanisms underlying pathological scarring by fibroblasts during wound healing.International wound journal · 2023Article
- Isorhamnetin attenuates the proliferation, invasion, migration and fibrosis of keloid fibroblasts by targeting S1PR1.Experimental and therapeutic medicine · 2023Article
- HDAC-an important target for improving tumor radiotherapy resistance.Frontiers in oncology · 2023Review
- Tissue chondrification and ossification in keloids with primary report of five cases.International wound journal · 2022Article
- CUDC907, a dual phosphoinositide-3 kinase/histone deacetylase inhibitor, promotes apoptosis of NF2 Schwannoma cells.Oncotarget · 2022Article
- Mechanotransduction in skin wound healing and scar formation: Potential therapeutic targets for controlling hypertrophic scarring.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloids are benign skin tumors with a high recurrence rate following surgical excision. Abnormal intracellular signaling is one of the key mechanisms involved in its pathogenesis. Over‑activated phosphoinositide 3‑kinase/RAC‑alpha serine/threonine‑protein kinase/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway and overproduction of histone deacetylases 2 (HDAC2) have also been observed in keloid fibroblasts (KFs). The present study aimed to explore the possibility of reversing the KF pathological phenotype using CUDC‑907, a dual inhibitor of PI3K/Akt/mTOR pathway and HDACs. KFs and keloid xenografts were treated with CUDC‑907 to examine its inhibitory effects on the pathological activities of KFs in vitro and in vivo. CUDC‑907 inhibited cell proliferation, migration, invasion and extracellular matrix deposition of in vitro cultured KFs and also suppressed collagen accumulation and disrupted the capillaries of keloid explants ex vivo and in vivo. A mechanistic study of CUDC‑907 revealed the initiation of cell cycle arrest at G2/M phase along with the enhanced expression of cyclin‑dependent kinase inhibitor 1 and decreased expression of cyclin B in cells treated with CUDC‑907. CUDC‑907 not only inhibited AKT and mTOR phosphorylation and promoted the acetylation of histone H3, but also significantly inhibited the phosphorylation levels of Smad2/3 and Erk. These preclinical data demonstrating its anti‑keloid effects suggest that CUDC‑907 may represent a candidate drug for systemic keloid therapy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.