ArticleCell communication and signaling : CCS2022
Transcription factor AP2 enhances malignancy of non-small cell lung cancer through upregulation of USP22 gene expression.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 23 citations in OpenAlex.
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- Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.American journal of cancer research · 2026Review
- Transcription factor TFAP2A drives the growth and metastasis and blocks ferroptosis of triple-negative breast cancer by activating PRAME transcription.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
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- TFAP2A induces cisplatin resistance via BNIP3-mediated mitophagy in non-small cell lung cancer.Translational cancer research · 2025Article
- TFAP2A facilitates the metastasis and radioresistance of esophageal cancer by promoting EGFR transcription.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- TFAP2A upregulates FAM83A to suppress ferroptosis and diminish cisplatin sensitivity in non-small cell lung cancer.Cell division · 2025Article
- Oncogenic Mutations and the Tumor Microenvironment: Drivers of Non-Small Cell Lung Cancer Progression.Cancers · 2025Review
- Identification of key regulators in pancreatic ductal adenocarcinoma using network theoretical approach.PloS one · 2025Article
- TFAP2A drives non-small cell lung cancer (NSCLC) progression and resistance to targeted therapy by facilitating the ESR2-mediated MAPK pathway.Cell death discovery · 2024Article
- Hepatocyte growth factor promotes melanoma metastasis through ubiquitin-specific peptidase 22-mediated integrins upregulation.Cancer letters · 2024Article
- Demethylzeylasteral induces PD-L1 ubiquitin-proteasome degradation and promotes antitumor immunityActa pharmaceutica Sinica. B · 2024Article
- How does exosome cause diabetes?Hormones (Athens, Greece) · 2024Review
- The Deubiquitinase USP22-Stabilized COL17A1 Promotes Lung Adenocarcinoma Progression.The clinical respiratory journal · 2024Article
- Ubiquitination and deubiquitination in cancer: from mechanisms to novel therapeutic approaches.Molecular cancer · 2024Review
- CRTAC1 identified as a promising diagnosis and prognostic biomarker in lung adenocarcinoma.Scientific reports · 2024Article
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- Inhibition of USP7 upregulates USP22 and activates its downstream cancer-related signaling pathways in human cancer cells.Cell communication and signaling : CCS · 2023Article
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
backgroundUbiquitin-specific protease 22 (USP22), a putative cancer stem cell marker, is frequently upregulated in cancers, and USP22 overexpression is associated with aggressive growth, metastasis, and therapy resistance in various human cancers including lung cancer. However, USP22 gene amplification seldom occurs, and the mechanism underlying USP22 upregulation in human cancers remains largely unknown.
methodsA luciferase reporter driven by a promoter region of USP22 gene was selectively constructed to screen against a customized siRNA library targeting 89 selected transcription factors to identify potential transcription factors (TFs) that regulate USP22 expression in human non-small cell lung cancers (NSCLC). Association of identified TFs with USP22 and potential role of the TFs were validated and explored in NSCLC by biological assays and immunohistochemistry analysis.
resultsLuciferase reporter assays revealed that SP1 and activating transcription factor 3 (ATF3) inhibit USP22 transcription, while transcription factor AP-2 Alpha/Beta (TFAP2A/2B) and c-Myc promote USP22 transcription. Binding site-directed mutagenesis and chromosome immunoprecipitation (ChIP) assays validated AP2α and AP2β are novel TFs of USP22. Furthermore, overexpression of AP2A and AP2B significantly upregulates USP22 expression, and its target: Cyclin D1, concurrently enhances the proliferation, migration, and invasion of NSCLC A549 and H1299 cells in a partially USP22-dependent manner. Moreover, AP2 protein level correlated with USP22 protein in human NSCLC tissues.
conclusionOur findings indicate AP2α and AP2β are important transcription factors driving USP22 gene expression to promote the progression of NSCLC, and further support USP22 as a potential biomarker and therapeutic target for lung cancer. Video Abstract.
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