ArticleCell death & disease2024
ADAMTS16 drives epithelial-mesenchymal transition and metastasis through a feedback loop upon TGF-β1 activation in lung adenocarcinoma.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- MZT2A drives epithelial-mesenchymal transition in lung adenocarcinoma via the LGALS3BP/ITGB1/TGF-β/smad2 axis.iScience · 2026Article
- Current Advances in the Physiological Roles and Disease-Associated Mechanisms of ADAMTS16.International journal of molecular sciences · 2026Review
- CPNE1 promotes stemness and confers resistance to GPC3 CAR-T cell therapy in hepatocellular carcinoma via the STAT3-TGF-β signaling pathway.Journal for immunotherapy of cancer · 2026Article
- YY1-induced upregulation of DLGAP5 promotes tumor progression in lung adenocarcinoma via Wnt/β-catenin/EMT pathway.Journal of translational medicine · 2026Article
- PTTG1-DLX2 axis drives malignant progression of lung adenocarcinoma by activating the WNT/β-catenin signaling pathway.Translational cancer research · 2026Article
- Biomarker identification of triple negative breast cancer subtypes using machine learning.NPJ systems biology and applications · 2026Article
- Development and multicenter validation of a predictive model for malignant pleural effusion recurrence.iScience · 2026Article
- The ADAMTS family: from extracellular matrix proteases to orchestrators of fibrosis.Cell communication and signaling : CCS · 2026Review
- A positive feedback loop between SERPINH1 and MMP-9/TGF-β1 promotes lung adenocarcinoma progression.Cell death and differentiation · 2026Article
- Network pharmacology analysis and in vitro experimental validation of liriodenine against non-small cell lung cancer.BMC cancer · 2025Article
- Article
- Deciphering the Role of ADAMTS6 in the Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Cells.International journal of molecular sciences · 2025Article
- Sorting nexin 9 expression and prognostic implications in lung adenocarcinoma: integrative bioinformatic andTranslational cancer research · 2025Article
- Interpretable Transfer Learning for Cancer Drug Resistance: Candidate Target Identification.Current issues in molecular biology · 2025Article
- ASAP1 Promotes Epithelial to Mesenchymal Transition by Activating the TGFβ Pathway in Papillary Thyroid Cancer.Cancer medicine · 2025Article
- SOX4 as a Key Oncogene Driving Tumor Invasion in Retinoblastoma.Investigative ophthalmology & visual science · 2025Article
- The role of TMEM59L in colorectal cancer progression and its interaction with the TGF-β/Smad pathway.Frontiers in oncology · 2025Article
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12 authors.
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Abstract
Lung adenocarcinoma (LUAD) is the major subtype of lung cancer. The poor prognosis of LUAD patients is attributed primarily to metastasis. ADAMTS16 is a crucial member of the ADAMTS family and is involved in tumor progression. However, its role and regulatory mechanism in LUAD remain unexplored. In this study, ADAMTS16 was identified as a crucial oncogene and survival predictor in LUAD via analyses of public datasets. Clinical specimens and tissue microarrays confirmed the differential expression and prognostic value of ADAMTS16 in LUAD patients. Transcriptome data and in vitro experiments demonstrated that ADAMTS16 was positively associated with epithelial-mesenchymal transition (EMT) and the migration abilities of LUAD cells. Knockdown of ADAMTS16 attenuated lung and pleural metastasis in an animal model. Mechanistically, the results of the enzyme-linked immunosorbent assay (ELISA) and western blot (WB) suggested that ADAMTS16 activated the TGF-β signaling pathway by facilitating the conversion of LAP-TGF-β1 to active TGF-β1. Co-Immunoprecipitation (co-IP) indicated an interaction between ADAMTS16 and LAP-TGF-β1. Inhibition of ADAMTS16 impaired EMT and aggressiveness of LUAD cells, while treatment with recombinant TGF-β1 reversed this inhibition. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays indicated that SOX4 acted as a transcriptional activator of ADAMTS16 and that TGF-β1 regulated the expression of ADAMTS16 by increasing the binding of SOX4 to the promoter of ADAMTS16. Suppressing the TGF-β signaling pathway inhibited ADAMTS16 expression, EMT, and lung metastasis, whereas overexpressing SOX4 reversed this inhibition. Therefore, ADAMTS16 forms a positive feedback loop with the TGF-β1/SOX4 axis to regulate EMT and metastasis, and disruption of this feedback loop inhibits tumor progression. These findings underscore the potential of ADAMTS16 as a prognostic biomarker and therapeutic target in LUAD and offer novel insight into the mechanism of EMT and metastasis.
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