Genomic instability induced by defects in the DNA damage response (DDR) network is a pivotal hallmark of cancer and a prime target for therapeutic intervention. Therapeutic strategies that exploit DDR defects using small-molecule inhibitors have shown increasing promise in targeted cancer therapy. The evolutionarily conserved dual-specificity tyrosine-regulated kinase (DYRK) family serves as a critical regulator of the DDR, yet the mechanisms linking DYRK activity to tumorigenesis and therapeutic response are only beginning to be elucidated. This review systematically summarizes the current knowledge regarding the involvement of DYRK kinases in DDR signaling and their impact on cancer progression. Furthermore, we comprehensively evaluate the landscape of existing DYRK inhibitors and discuss their promising applications in cancer treatment. By elucidating the functional interplay between DYRKs and the DDR machinery, this review advances our understanding of these kinases and highlights the rationale for exploiting DYRK inhibition as a promising strategy in precision oncology.
Cao et al. (Sun,) studied this question.
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