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Keywords {🔍}

usp, cancer, lung, cells, expression, pubmed, cell, transcription, article, google, scholar, cas, promoter, fig, luciferase, gene, cmyc, protein, activity, data, tissues, analysis, overexpression, binding, apβ, central, factor, region, factors, knockdown, panel, atf, mrna, found, transcriptional, human, apα, zhang, sirna, tfs, nsclc, tfapa, site, reporter, proliferation, dna, shown, wang, proteins, adenocarcinoma,

Topics {✒️}

usp22/wnt/beta-catenin signaling axis sirt1/akt/mrp1 signaling pathway usp22-promoter-driven luciferase activity gene-specific sirnas targeting dnapk-mediated gammah2ax formation c-myc promote usp22 transcription nf-kappab signaling pathway dna-damage-repair pathways ku70/bax-mediated apoptosis renilla-luciferase expressing plasmid ubiquitin-specific protease 22 dna double-strand breaks dual-luciferase reporter system purified protein-dna complexes account cell communication positive feedback loop partially usp22-dependent manner cross-linked protein-dna crispr/cas 9 system luciferase reporter driven usp22 transcription start site binding site-directed mutagenesis wild type promoter histone ubiquitination dependent vegf/pedf signaling mono-ubiquitin moiety histone-modifying enzyme cell stem cell cox-2 signaling pathway privacy choices/manage cookies luciferase reporters driven activating transcription factor 3 customized sirna library selected transcription factors gene-specific sirna nuclear transcription factor pka/creb regulates sirna library targeting authors scientific editing important negative regulator bmc widely accepted finding ap2 enhances malignancy human lung carcinoma a549 cell lines c-myc knockdown resulted renilla luciferase activity transcription regulatory elements human lung adenocarcinoma cell signaling technology

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         description:Ubiquitin-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. A 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. Luciferase 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. Our 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.
         datePublished:2022-09-19T00:00:00Z
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      headline:Transcription factor AP2 enhances malignancy of non-small cell lung cancer through upregulation of USP22 gene expression
      description:Ubiquitin-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. A 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. Luciferase 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. Our 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.
      datePublished:2022-09-19T00:00:00Z
      dateModified:2022-09-19T00:00:00Z
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         USP22
         AP2
         ATF3
         NSCLC
         Transcriptional regulation
         Cell proliferation
         Invasion
         Malignancy
         Cell Biology
         Protein-Ligand Interactions
         Receptors
         Cytokines and Growth Factors
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