Abstract
Gynaecological cancers are attributed to the second most diagnosed cancers in women after breast cancer. On a global scale, cervical cancer is the fourth most common cancer and the most common cancer in developing countries with rapidly increasing mortality rates. Human papillomavirus (HPV) infection is a major contributor to the disease. HPV infections cause prominent cellular changes including alternative splicing to drive malignant transformation. A fundamental characteristic attributed to cancer is the dysregulation of cellular transcription. Alternative splicing is regulated by several splicing factors and molecular changes in these factors lead to cancer mechanisms such as tumour development and progression and drug resistance. The serine/arginine-rich (SR) proteins and heterogeneous ribonucleoproteins (hnRNPs) have prominent roles in modulating alternative splicing. Evidence shows molecular alteration and expression levels in these splicing factors in cervical cancer. Furthermore, aberrant splicing events in cancer-related genes lead to chemo- and radioresistance. Identifying clinically relevant modifications in alternative splicing events and splicing variants, in cervical cancer, as potential biomarkers for their role in cancer progression and therapy resistance is scrutinised. This review will focus on the molecular mechanisms underlying the aberrant splicing events in cervical cancer that may serve as potential biomarkers for diagnosis, prognosis, and novel drug targets.
Highlights
Cervical cancer, known as cervix uteri cancer, is the fourth most frequently diagnosed cancer globally and the most common malignancy in developing countries [1]
This study revealed the direct interaction of hnRNPA1 and hnRNPA2 with high-risk HPV16 splice site SA742 and SA409
The development of cervical cancer is largely influenced by Human papillomavirus (HPV) infections in low- and middleincome countries that add to this encumbrance
Summary
Known as cervix uteri cancer, is the fourth most frequently diagnosed cancer globally and the most common malignancy in developing countries [1]. HPV is a circular double-stranded DNA virus with capsid proteins with more than 200 subtypes identified and categorised as high and low risk. Persistent infection with these high-risk subtypes contributes to over 99% of cervical cancers [11]. Novel therapeutic targets are warranted to address this issue Prevention strategies such as HPV vaccinations and pap smears play a significant role in cervical cancer prevention. This review will focus on the molecular mechanisms underlying the aberrant splicing events in cervical cancer that may serve as potential biomarkers for diagnosis and prognosis and as novel drug targets for their therapeutic properties
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