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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Cdc6 expression is induced by HPV16 E6 and E7 oncogenes and represses E-cadherin expression
E Faghihloo1, M Sadeghizadeh2, S Shahmahmoodi3
1Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Cancer Gene Therapy
|November 12, 2016
Summary
Human papillomavirus (HPV) oncoproteins E6 and E7 reduce E-cadherin expression in cervical cancer cells. Cdc6 (cell division cycle 6) overexpression, induced by these oncoproteins, is key to E-cadherin suppression and potential metastasis.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Cervical cancer, a common malignancy in women, is linked to high-risk human papillomaviruses (HPVs) and their oncoproteins E6 and E7.
- E-cadherin downregulation is implicated in epithelial-to-mesenchymal transition (EMT) and cancer progression, but its mechanism in cervical cancer remains unclear.
Purpose of the Study:
- To investigate the impact of HPV16 E6 and E7 oncoproteins on E-cadherin and Cdc6 (cell division cycle 6) expression.
- To elucidate the role of Cdc6 in HPV-associated E-cadherin suppression.
Main Methods:
- Utilized the HCT-116 cell line expressing HPV16 E6 and/or E7 oncoproteins.
- Assessed E-cadherin and Cdc6 expression levels.
- Employed short hairpin RNA (shRNA) to suppress Cdc6 expression.
Main Results:
- HPV16 E6 and E7 significantly reduced E-cadherin expression, with E6 causing a more pronounced effect.
- Both E6 and E7 oncoproteins induced Cdc6 expression, with E6 showing greater induction.
- Cdc6 suppression via shRNA restored E-cadherin levels, indicating its critical role.
Conclusions:
- Cdc6 overexpression is a significant factor in E-cadherin reduction in HPV16 E6/E7-expressing cells.
- Cdc6 may play a crucial role in the metastasis of HPV-associated cancers.
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