ArticleJournal of experimental & clinical cancer research : CR2022
HDAC7 promotes NSCLC proliferation and metastasis via stabilization by deubiquitinase USP10 and activation of β-catenin-FGF18 pathway.
Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
- PHLDA1 knockdown exacerbates emphysema in COPD by attenuating proliferation of alveolar type II cells via modulating GLI1 nuclear translocation.Cellular and molecular life sciences : CMLS · 2026Article
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- Fibroblast-mediated KRAS activation in double-negative prostate cancer.Cell death & disease · 2026Article
- Histone deacetylases: Function in tumor development and therapeutic prospects (Review).Oncology letters · 2026Review
- The role and mechanism of histone deacetylase in COPD.Molecular and cellular biochemistry · 2026Review
- ADAT2-mediated A-to-I tRNA modification promotes oncogenic translation and colorectal cancer progression and chemoresistance.Molecular cancer · 2026Article
- Review
- Ubiquitination and deubiquitination as critical modulators of NSCLC tumorigenesis and drug resistance.Discover oncology · 2026Review
- Differential transcriptomic modulation by histone deacetylase inhibitor SAHA in LUAD and LUSC.Clinical epigenetics · 2026Article
- Co-targeting MRPS7-23 synergistically enhances cisplatin efficacy to suppress nasopharyngeal carcinoma growth and metastasis.International journal of biological sciences · 2026Article
- Role of the SOX family in non‑small cell lung cancer: Molecular mechanisms and therapeutic implications (Review).Oncology reports · 2026Review
- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- Histone deacetylase HDAC7 restricts CD8 + T cell tumor infiltration and limits immunotherapy sensitivity in bladder cancer: reversal by pinocembrin.Journal of experimental & clinical cancer research : CR · 2025Article
- Modified Xiao-Qing-Long-decoction prevents inflammation and promotes Nur77 expression in mice with acute respiratory distress syndrome by inhibiting HDAC7 expression.Pharmaceutical biology · 2025Article
- HDAC1/2-mediated deacetylation of KLF9 promotes the malignant progression of nasopharyngeal carcinoma via CDH17.Oncogene · 2025Article
- HDAC7 promotes renal cancer progression by reprogramming branched-chain amino acid metabolism.Science advances · 2025Article
- Nuclear to Cytoplasmic Transport Is a Druggable Dependency in HDAC7-driven Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Discovery of a potential hematologic malignancies therapy: Selective and potent HDAC7 PROTAC degrader targeting non-enzymatic function.Acta pharmaceutica Sinica. B · 2025Article
- Scaffolding Activities of Pseudodeacetylase HDAC7.ACS chemical biology · 2025Review
- Fibroblast Growth Factors: Roles and Emerging Therapeutic Applications.Current drug targets · 2025Review
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Authors and funding
17 authors at 10 institutions in 4 countries.
Funding
Abstract
backgroundHistone deacetylases (HDACs) play crucial roles in cancers, but the role and mechanism of HDAC7 in NSCLC have not been fully understood.
methodsA total of 319 patients with non-small cell lung cancer (NSCLC) who underwent surgery were enrolled in this study. Immunohistochemistry and Kaplan-Meier survival analysis were performed to investigate the relationship between HDAC7, fibroblast growth factor 18 (FGF18) expression, and clinicopathologic characteristics. Cell functional experiments were implemented both in vivo and in vitro to investigate the effects on NSCLC cell proliferation and metastasis. Recombinant lentivirus-meditated in vivo gene overexpression or knockdown, real-time polymerase chain reaction (PCR), western blotting, and coimmunoprecipitation assays were applied to clarify the underlying molecular mechanism of HDAC7 in promoting NSCLC progression.
resultsThe elevated expression of HDAC7 or FGF18 was positively correlated with poor prognosis, tumor-node-metastasis (TNM) stage, and tumor differentiation of NSCLC patients. NSCLC patients with co-expressed HDAC7 and FGF18 suffered the worst prognosis. HDAC7 overexpression promoted NSCLC proliferation and metastasis by upregulating FGF18. Conversely, overexpression of FGF18 reversed the attenuated ability in tumor growth and metastasis mediated by downregulating HDAC7. In terms of mechanism, our results suggested that the interaction of HDAC7 with β-catenin caused decreased β-catenin acetylation level at Lys49 and decreased phosphorylation level at Ser45. As a consequence, the HDAC7-mediated posttranslational modification of β-catenin facilitated nuclear transfer and activated FGF18 expression via binding to TCF4. Furthermore, deubiquitinase USP10 interacted with and stabilized HDAC7. The suppression of USP10 significantly accelerated the degradation of HDAC7 and weakened NSCLC growth and migration.
conclusionsOur findings reveal that HDAC7 promotes NSCLC progression through being stabilized by USP10 and activating the β-catenin-FGF18 pathway. Targeting this novel pathway may be a promising strategy for further developments in NSCLC therapy.
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