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 chemoand
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.