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Updated: Feb 2, 2026
Chromogenic In Situ Hybridization as a Tool for HPV-Related Head and Neck Cancer Diagnosis
Published on: June 14, 2019
Aurora kinases are a novel therapeutic target for HPV-positive head and neck cancers
Mushfiq H Shaikh1, Adi Idris2, Newell W Johnson3
1Menzies Health Institute Queensland, School of Dentistry and Oral Health, Griffith University, Southport, Queensland, Australia; Menzies Health Institute Queensland, School of Medical Science, Griffith University, Southport, Queensland, Australia.
Objectives:
Human papilloma virus (HPV) is the main culprit in cancers of the cervix, penis, anus, skin, eye and head and neck. Current treatments for HPV cancers have not altered survival outcomes for 30 years and there is a significant lack of targeted therapeutic agents in the management of advanced HPV-related HNSCC. Here we show that survival and maintenance of HPV-positive HNC cells relies on the continuous expression of the major HPV oncogene, E7, and that Aurora kinases are critical for survival of high-risk HPV-positive HNC cells.
Materials And Methods:
To assess the role of HPV E7 on HNC cell survival, RNA interference (RNAi) of the E7 gene was initially performed. Using an Aurora kinase inhibitor, Alisertib, the role of Aurora kinases in the carcinogenesis of HPV E7 positive HNC tumour lines was then investigated. An in vivo HNC xenograft model was also utilised to assess loss of tumour volume in response to RNAi E7 gene silencing and Alisertib treatment.
Results:
RNAi silencing of the HPV E7 gene inhibited the growth of HPV-positive HNC cells and in vivo tumour load. We show that HPV E7 oncogene expression confers sensitivity to Alisertib on HNC cells where Alisertib-mediated loss in in vitro cell viability and in vivo tumour load is dependent on E7 expression. Moreover, Aurora kinase inhibition induced degradation of MCL-1 in HPV E7-expressing HNC cells.
Conclusion:
Overall, we show that Aurora kinases are a novel therapeutic target for HPV-positive HNCs. It might be feasible to combine Aurora kinase and MCL-1 inhibitors for future HNC therapies.
Insights
Human papilloma virus (HPV) oncogene E7 drives cancer cell survival. Aurora kinase inhibition, using Alisertib, effectively reduces tumor growth in HPV-positive head and neck cancers.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Human papilloma virus (HPV) is a primary cause of various cancers, including head and neck squamous cell carcinoma (HNSCC).
- Existing treatments for HPV-related cancers have shown limited impact on survival rates for decades.
- There is a critical need for targeted therapies against advanced HPV-positive HNSCC.
Purpose of the Study:
- To investigate the role of the HPV E7 oncogene in the survival of HPV-positive head and neck cancer (HNC) cells.
- To determine if Aurora kinases are essential for the survival of high-risk HPV-positive HNC cells.
- To evaluate the efficacy of Aurora kinase inhibition as a therapeutic strategy for HPV-positive HNC.
Main Methods:
- RNA interference (RNAi) was used to silence the HPV E7 gene.
- An Aurora kinase inhibitor, Alisertib, was employed to study its effects on HPV-positive HNC cell lines.
- An in vivo HNC xenograft model was utilized to assess tumor response to E7 gene silencing and Alisertib treatment.
Main Results:
- Silencing of the HPV E7 gene significantly inhibited the growth of HPV-positive HNC cells and reduced in vivo tumor load.
- HPV E7 oncogene expression rendered HNC cells sensitive to Alisertib, leading to decreased cell viability and tumor load.
- Inhibition of Aurora kinases by Alisertib induced the degradation of MCL-1 in HPV E7-expressing HNC cells.
Conclusions:
- Aurora kinases represent a novel therapeutic target for HPV-positive HNCs.
- Combining Aurora kinase inhibitors with MCL-1 inhibitors may offer a promising future therapeutic approach for HNC.
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