ArticleCancer cell international2019
Secretory leukocyte protease inhibitor suppresses HPV E6-expressing HNSCC progression by mediating NF-κB and Akt pathways.
Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Targeting the STK39/ARID2 Axis to Inhibit NF-κB Signaling: A Novel Pathway for Mesenchymal Stem Cell Osteogenic Differentiation in Osteoporosis Management.Journal of musculoskeletal & neuronal interactions · 2026Article
- SLPI in Prostate Cancer.Cancers · 2026Review
- HPV16-miR-H1 promotes proliferation, migration, and glycolysis in head and neck squamous cell carcinoma cells via the PTEN/AKT pathway.Scientific reports · 2025Article
- Article
- Roles of human papillomavirus in cancers: oncogenic mechanisms and clinical use.Signal transduction and targeted therapy · 2025Review
- Cationic Liposomes Carrying HPV16 E6-siRNA Inhibit the Proliferation, Migration, and Invasion of Cervical Cancer Cells.Pharmaceutics · 2024Article
- Review
- PI3K/AKT/mTOR Signaling Pathway in HPV-Driven Head and Neck Carcinogenesis: Therapeutic Implications.Biology · 2023Review
- Evolving landscape of PD-L2: bring new light to checkpoint immunotherapy.British journal of cancer · 2023Review
- Proteases and HPV-Induced Carcinogenesis.Cancers · 2022Review
- CircRFWD3 promotes HNSCC metastasis by modulating miR-27a/b/PPARγ signaling.Cell death discovery · 2022Article
- HPV16 E6 enhances the radiosensitivity in HPV-positive human head and neck squamous cell carcinoma by regulating the miR-27a-3p/SMG1 axis.Infectious agents and cancer · 2021Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHead and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide and human papillomavirus (HPV) has been increasingly recognized as a pathogenic factor for the initiation and development of HNSCC. E6 oncogene, an essential component of the HPV 16 virus, acts as a leading cause of the malignant transformation of cancer cells. Therefore, investigating the biological effect and potential mechanisms of E6 oncogene on HNSCC cells and exploring potential therapeutic methods is of great value.
methodsMTT assay, cell cycle analysis, and apoptosis assay were implemented to detect the biological effect of E6 oncogene on the growth of HNSCC cells. Wound healing assay and transwell assay were used to evaluate the role of E6 in the migration and invasion of HNSCC cells. Western blot and immunofluorescence assay were adopted to explore the regulatory mechanisms underlying E6-induced HNSCC progression. Then, exogenous secretory leukocyte protease inhibitor (SLPI) was added into the cell culture to investigate whether it could maintain its tumor suppressor effect on E6-expressing HNSCC cells.
resultsHPV E6 oncogene could promote the proliferation, cell cycle period, apoptosis resistance, migration and invasion of HNSCC cells by activating NF-κB and Akt pathways. Immunohistochemical analysis conducted on HNSCC tissues illustrated that SLPI was further downregulated in HPV positive HNSCC compared to HNSCC without HPV infection. Exogenous SLPI significantly inhibited HPV E6-mediated malignant phenotypes in HNSCC cells by inhibiting the activation of NF-κB and Akt and signaling pathways.
conclusionsThis study demonstrated that E6 oncogene led to the malignant transformation of HNSCC cells by regulating multiple pathways. SLPI could reverse the effect of E6 oncogene on HNSCC, implying that the functional inhibition of E6 by SLPI may be exploited as an attractive therapeutic strategy.
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