Globally

cervical cancer (CxCa) ranks 4th common cancer among females and led to 569

847 incidences and 311

365 deaths in 2018. 80% of CxCa cases occur due to persistent infection with a high-risk subtype of human papillomavirus (HPV-16 and 18). Smoking

high parity

and co-infection with type 2 herpes simplex or HIV are other known risk factors for CxCa. Major histological subtypes are squamous (70%) and adenocarcinoma (25%). Presently

concurrent radiation plus cisplatin (CDDP)-based chemotherapy is the standard treatment for CxCa patients. However

CDDP resistance and toxic side effects limit its efficacy

leading to a poorer response rate and an expected overall survival ranging from 10 to 17.5 months. Reduced drug uptake

increased DNA damage repair

increased CDDP inactivation

and overexpressed Bcl-2 or caspase inhibition

are primarily accountable mechanisms for CDDP resistance and improving CDDP’s efficacy remains the major challenge. Poly (ADP-ribosyl) polymerase-1

an effective mediator of nucleotide excision repair pathway

is involved in DNA repair as well as maintaining genomic stability and is significantly expressed in malignant lymphomas

hepatocellular-

cervical- and colorectal carcinoma

which has been approved effective in maintenance therapy and may serve as an effective target to enhance CDDP sensitivity in CxCa. Here

we summarize the etiology and epidemiology of and treatment for CxCa

the mechanism responsible for chemotherapy resistance

PARP inhibitor as a possible therapy for CxCa

and other possible chemotherapeutic options for CxCa treatment.