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. 2026 Mar 23;19:583883. doi: 10.2147/OTT.S583883

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© 2026 Xu and Gao.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v4.0) License (http://creativecommons.org/licenses/by-nc/4.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

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Schematic overview of the dual regulatory mechanisms by which SIK2 promotes HRR and chemotherapy resistance in ovarian cancer. SIK2 drives HRR proficiency via two parallel axes: (1) direct phosphorylation of RAD50 at Ser635 to promote RAD50-mediated DSBs repair; (2) phosphorylation of class-IIa HDACs (HDAC4/5/7) to sustain MEF2D transcriptional activity and upregulate HRR-related gene expression. These pathways converge to repair chemotherapy-induced DSBs, preventing tumor cell apoptosis and driving chemoresistance.

Abbreviations: SIK2, Salt-inducible kinase 2; HRR, Homologous recombination repair; Ser635, Serine 635; DSBs, DNA double-strand breaks; HDACs, Histone deacetylases; MEF2D, Myocyte enhancer factor 2D.