Journal
CANCER LETTERS
Volume 496, Issue -, Pages 104-116Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2020.10.004
Keywords
Cytidine deaminase; DNA/RNA editing; HPV; Viral restriction; Mutation
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Funding
- NIG-JOINT [1A2019]
- University Grant Commission, Government of India
- DST-FIST grant
- UGC-SAP grant
- DHR-MRU grant
- DBT
- ICMR
- DAE-BRNS, Government of India
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Cervical cancer, a common cancer in women, is primarily caused by HPV infection. Apart from genetic and epigenetic factors, the APOBEC3 family plays a crucial role in the molecular pathogenesis of cancer, including inducing tumor mutations through DNA editing mechanisms.
Cervical cancer is one of the foremost common cancers in women. Human papillomavirus (HPV) infection re-mains a major risk factor of cervical cancer. In addition, numerous other genetic and epigenetic factors also are involved in the underlying pathogenesis of cervical cancer. Recently, it has been reported that apolipoprotein B mRNA editing enzyme catalytic polypeptide like (APOBEC), DNA-editing protein plays an important role in the molecular pathogenesis of cancer. Particularly, the APOBEC3 family was shown to induce tumor mutations by aberrant DNA editing mechanism. In general, APOBEC3 enzymes play a pivotal role in the deamination of cytidine to uridine in DNA and RNA to control diverse biological processes such as regulation of protein expression, innate immunity, and embryonic development. Innate antiviral activity of the APOBEC3 family members restrict retroviruses, endogenous retro-element, and DNA viruses including the HPV that is the leading risk factor for cervical cancer. This review briefly describes the pathogenesis of cervical cancer and discusses in detail the recent findings on the role of APOBEC in the molecular pathogenesis of cervical cancer.
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