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Targeting androgen receptor (AR) is effective against prostate cancer (PC), but frequently leads to development of incurable castration\u2010resistant PC (CRPC). We show that emergence of CRPC is associated with significant upregulation of CDK2 cyclins and downregulation of CDK4\/6 cyclins. This rewiring renders CRPC cells dependent on the high CDK2 activity, and CDK2\u2010specific inhibitors efficiently decrease proliferation of PC and CRPC cells. We develop a CDK2 inhibitor\u2010resistant CRPC model and perform a rational compound screen to assess which of the currently used anti\u2010CRPC treatments could augment CDK2 therapy\u2010response. This dual approach revealed that when our CRPC model acquired resistance to CDK2 inhibition, it increased AR signaling, and the combination of CDK2 inhibition with anti\u2010androgens induces synergistic antiproliferative effects on CRPC cells. Importantly, CDK2 inhibitors also show synergistic interaction with cell cycle poisons such as Docetaxel and Cisplatin, and combinatorial effects are also seen with radiotherapy, thereby offering multiple combinations against CRPC. In brief, we propose that CDK2 inhibition provides a rational basis for combinatorial therapy against CRPC.<\/jats:p>","DOI":"10.1002\/1878-0261.70319","type":"journal-article","created":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T11:09:11Z","timestamp":1788347351000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Castration\u2010resistant prostate cancer cells are addicted to the high activity of cyclin\u2010dependent kinase 2"],"prefix":"10.1002","author":[{"given":"Joyeeta","family":"Chatterjee","sequence":"first","affiliation":[{"name":"Department of Clinical Molecular Biology, EpiGen Institute of Clinical Medicine, University of Oslo  Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessia","family":"Marin","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Developmental Biology, Faculty of Medicine University of Helsinki  Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shivani","family":"Yalala","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Developmental Biology, Faculty of Medicine University of Helsinki  Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5194-7064","authenticated-orcid":false,"given":"Harri M.","family":"Itkonen","sequence":"additional","affiliation":[{"name":"Department of Clinical Molecular Biology, EpiGen Institute of Clinical Medicine, University of Oslo  Norway"},{"name":"Department of Biochemistry and Developmental Biology, Faculty of Medicine University of Helsinki  Finland"},{"name":"EpiGen, Medical Division Akershus University Hospital  L\u00f8renskog Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,2]]},"reference":[{"issue":"1","key":"e_1_2_11_2_1","first-page":"10","article-title":"Cancer 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