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Key Molecular Events in Cervical Cancer Development.
Shandra Devi Balasubramaniam1, Venugopal Balakrishnan1, Chern Ein Oon1
1Institute for Research in Molecular Medicine, Universiti Sains Malaysia, 11800 Minden, Pulau Pinang, Malaysia.
Medicina (Kaunas, Lithuania)
|July 20, 2019
Summary
High-risk human papillomavirus (HPV) drives cervical cancer by disrupting tumor suppressor proteins like p53 and pRb. This leads to uncontrolled cell growth and genomic instability, promoting cancer progression.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Cervical cancer is a significant global health issue for women.
- High-risk human papillomavirus (HPV) infection is the primary cause of cervical cancer.
- HPV genome integration into host cells initiates neoplastic progression.
Purpose of the Study:
- To review the key molecular events in cervical carcinogenesis.
- To explain the role of HPV oncoproteins E6 and E7.
- To discuss the disruption of tumor suppressor proteins p53 and pRb.
Main Methods:
- Review of existing literature on cervical cancer molecular pathogenesis.
- Analysis of the mechanisms of HPV oncoprotein action.
- Examination of gene expression changes in cervical intraepithelial neoplasia (CIN) and cancer.
Main Results:
- HPV oncoproteins E6 and E7 inactivate p53 and pRb, crucial tumor suppressors.
- Inactivation of p53 and pRb impairs DNA repair and apoptosis, promoting cell proliferation.
- Increased expression of genes involved in DNA repair, proliferation, angiogenesis, and mitogenesis occurs.
Conclusions:
- HPV infection initiates cervical carcinogenesis through viral oncoprotein activity.
- Genomic instability resulting from disrupted cellular mechanisms drives cancer progression.
- Understanding these molecular events is crucial for developing targeted therapies.
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