ArticleJournal of translational medicine2014
Down-regulation of Sp1 suppresses cell proliferation, clonogenicity and the expressions of stem cell markers in nasopharyngeal carcinoma.
Article in Journal of translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- SP1 Expression and the Clinicopathological Features of Tumors: A Meta-Analysis and Bioinformatics Analysis.Pathology oncology research : POR · 2021Pooled it
- Clofarabine Enhances the Transduction Efficiency of Recombinant AAV2 in the Retina.Investigative ophthalmology & visual science · 2025Article
- TF Profiler: a transcription factor inference method that broadly measures transcription factor activity and identifies mechanistically distinct networks.Genome biology · 2025Article
- SP1/RNASEH2A accelerates the development of hepatocellular carcinoma by regulating EMT.Heliyon · 2023Article
- Sp1 Upregulation Bolsters the Radioresistance of Glioblastoma Cells by Promoting Double Strand Breaks Repair.International journal of molecular sciences · 2023Article
- miR-145-5p Targets Sp1 in Non-Small Cell Lung Cancer Cells and Links to BMI1 Induced Pemetrexed Resistance and Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2022Article
- Exploring the Novel Computational Drug Target and Associated Key Pathways of Oral Cancer.Current issues in molecular biology · 2022Article
- Epigenetic clock and methylation studies in vervet monkeys.GeroScience · 2022Article
- Down-syndrome-induced senescence disrupts the nuclear architecture of neural progenitors.Cell stem cell · 2022Article
- Intricate crosstalk between MYB and noncoding RNAs in cancer.Cancer cell international · 2021Review
- DNA methylation age analysis of rapamycin in common marmosets.GeroScience · 2021Article
- miR-9 modulates and predicts the response to radiotherapy and EGFR inhibition in HNSCC.EMBO molecular medicine · 2021Article
- High copy number variations, particular transcription factors, and low immunity contribute to the stemness of prostate cancer cells.Journal of translational medicine · 2021Article
- Transcriptional control of parturition: insights from gene regulation studies in the myometrium.Molecular human reproduction · 2021Review
- SP1-induced AFAP1-AS1 contributes to proliferation and invasion by regulating miR-497-5p/CELF1 pathway in nasopharyngeal carcinoma.Human cell · 2021Article
- The miR-25-3p/Sp1 pathway is dysregulated in ovarian endometriosis.The Journal of international medical research · 2020Article
- SP1/AKT/FOXO3 Signaling Is Involved in miR-362-3p-Mediated Inhibition of Cell-Cycle Pathway and EMT Progression in Renal Cell Carcinoma.Frontiers in cell and developmental biology · 2020Article
- Article
- Direct and Indirect Targeting of HOXA9 Transcription Factor in Acute Myeloid Leukemia.Cancers · 2019Review
- MicroRNA-1258, regulated by c-Myb, inhibits growth and epithelial-to-mesenchymal transition phenotype via targeting SP1 in oral squamous cell carcinoma.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTranscription factor Sp1 is multifaceted, with the ability to function as an oncogene or a tumor suppressor, depending on the cellular context. We previously reported that Sp1 is required for the transcriptional activation of the key oncogenes in nasopharyngeal carcinoma (NPC), including B-lymphoma mouse Moloney leukemia virus insertion region 1 (Bmi1) and centromere protein H (CENPH), but the role of Sp1 and its underlying mechanisms in NPC remained largely unexplored. The objective of this study was to investigate the cellular function of Sp1 and to verify the clinical significance of Sp1 as a potential therapeutic target in NPC.
methodsThe levels of Sp1 in the normal primary nasopharyngeal epithelial cells (NPECs) and NPC cell lines were analyzed by Quantitative Real-time RT-PCR (qRT-PCR) and Western blot. The location and expression of Sp1 in the NPC tissues were detected by immunohistochemistry staining (IHC). The effect of Sp1 knockdown on the cell proliferation, clonogenicity, anchorage-independent growth and the stem-cell like phenotype in NPC cells were evaluated by MTT, flow cytometry, clonogenicity analysis and sphere formation assay.
resultsThe mRNA and protein levels of Sp1 were elevated in NPC cell lines than in the normal primary NPECs. Higher expression of Sp1 was found in NPC tissues with advanced clinical stage (P=0.00036). Either inhibition of Sp1 activity by mithramycin A, the FDA-approved chemotherapeutic anticancer drug or Sp1 silencing by two distinct siRNA against Sp1 suppressed the growth of NPC cells. Mechanism analysis revealed that Sp1 silencing may suppress cell proliferation, clonogenicity, anchorage-independent growth and the stem-cell like phenotype through inducing the expression of p27 and p21, and impairing the expressions of the critical stem cell transcription factors (SCTFs), including Bmi1, c-Myc and KLF4 in NPC cells.
conclusionsSp1 was enriched in advanced NPC tissues and silencing of Sp1 significantly inhibited cell proliferation, clonogenicity, anchorage-independent growth and the stem-cell like phenotype of NPC cells, suggesting Sp1 may serve as an appealing drug target for NPC.
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