Mechanisms and Reversal Strategies of Drug Resistance in Targeted Therapy for Cervical Cancer: Anti-angiogenic Agents and PARP Inhibitors

Abstract

Drug resistance to anti-angiogenic agents and PARP inhibitors in cervical cancer targeted therapy severely restricts clinical efficacy. This paper systematically analyzes the resistance mechanisms of these two classes of drugs: Anti-angiogenic drug resistance is associated with hypoxia-induced compensatory activation of the VEGF pathway, metabolic reprogramming, and epithelial-mesenchymal transition (EMT) in the tumor microenvironment; PARP inhibitor resistance originates from BRCA1/2 gene reversion mutations, reconstruction of DNA damage repair pathways, and enhanced cancer stem cell properties. Targeting these mechanisms, reversal strategies including combination therapy, precision medication, and nanodelivery systems are proposed to provide a theoretical basis for overcoming drug resistance in clinical practice.