MEK/ERK signaling is a critical regulator of high-risk human papillomavirus oncogene expression revealing therapeutic targets for HPV-induced tumors
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View abstract on PubMed
Summary
This summary is machine-generated.High-risk human papillomaviruses (hr-HPVs) use EGFR/MEK/ERK signaling to drive oncogene expression and cancer. Inhibiting this pathway halts HPV oncogene transcription and the neoplastic phenotype, offering a potential treatment for HPV-induced cancers.
Area Of Science
- Oncology
- Virology
- Cell Signaling
Background
- Intracellular pathogens, including high-risk human papillomaviruses (hr-HPVs), can hijack cellular processes, leading to cancer.
- While hr-HPV oncogenes E6 and E7 are known drivers of malignancy, the regulation of their transcription remains unclear.
Purpose Of The Study
- To investigate the mechanisms regulating hr-HPV oncogene transcription.
- To explore the role of EGFR/MEK/ERK signaling in hr-HPV-induced neoplastic progression.
- To identify potential therapeutic targets for HPV-associated cancers.
Main Methods
- Utilized monolayer cell cultures, epithelial organotypic tissue models, and neoplastic tissue biopsies.
- Investigated the impact of epithelial contact inhibition and differentiation on hr-HPV oncogene expression.
- Assessed the role of EGFR/MEK/ERK signaling and AP-1 transcription factors.
- Evaluated the efficacy of pharmacological inhibitors of EGFR, MEK, and ERK signaling.
Main Results
- Epithelial contact inhibition and differentiation normally suppress hr-HPV oncogene expression.
- EGFR/MEK/ERK signaling activation overrides cellular controls, promoting HPV oncogene transcription and neoplastic phenotype.
- EGFR/MEK/ERK signaling influences AP-1 transcription factor activity, which is crucial for oncogene transcription.
- Pharmacological inhibition of EGFR, MEK, and ERK signaling effectively suppressed HPV oncogene expression and neoplastic characteristics.
Conclusions
- hr-HPVs exploit the EGFR/MEK/ERK signaling pathway for oncogene regulation and productive replication.
- Targeting the EGFR/MEK/ERK pathway presents a promising therapeutic strategy for treating HPV-induced neoplasia and cancers.
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