Abstract
Tumor resistance is one of the primary reasons for cancer treatment failure, significantly limiting the options and efficacy of cancer therapies. Therefore, overcoming resistance has become a critical factor in improving cancer treatment outcomes. IGF2BP2, as a reader of m6A methylation, plays a pivotal role in the post-transcriptional regulation of RNA through the methylation of m6A sites. It not only contributes to cancer initiation and progression but also plays a key role in tumor drug resistance. This review provides a comprehensive summary of the mechanisms by which IGF2BP2 contributes to therapy resistance, with the aim of improving the efficacy of chemotherapy in cancer treatment. Advancing research in this area is crucial for developing more effective therapies that could significantly improve the quality of life for cancer patients.