Evidence map›Paper›PMID 42397909›Full record

ArticleScience advances2026

Cyclin K condensates bridge CDK12 to phosphorylate and drive oncogenic YAP activation in hepatocellular carcinoma.

Yang Sun, Yu Zhang, Weikang Yan, Jinlin Duan, Ke Qiao, Guoquan Yan, Junyan Xue, Jie Wang, Ming Zhan, Qiwei Li and 2 more

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Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Yang SunLaboratory of Targeted Therapy and Precision Medicine, Department of Clinical Laboratory, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0009-0003-6078-672X
Yu ZhangLaboratory of Targeted Therapy and Precision Medicine, Department of Clinical Laboratory, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0009-0007-7399-0200
Weikang YanDepartment of Biliary-Pancreatic Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0003-4789-9925
Jinlin DuanDepartment of Pathology, Tongren Hospital Shanghai Jiaotong University School of Medicine, Shanghai, China.
Ke QiaoShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, China.
Guoquan YanInstitute of Biomedical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Junyan XueLaboratory of Targeted Therapy and Precision Medicine, Department of Clinical Laboratory, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Jie WangLaboratory of Targeted Therapy and Precision Medicine, Department of Clinical Laboratory, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.
Ming ZhanDepartment of Systems Biology, Beckman Research Institute, City of Hope, Monrovia, CA 91016, USA.ORCID 0000-0002-4668-727X
Qiwei LiDepartment of Biliary-Pancreatic Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Hongcheng WangDepartment of General Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0000-8548-5198
Yonglong ZhangLaboratory of Targeted Therapy and Precision Medicine, Department of Clinical Laboratory, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China.ORCID 0000-0001-6429-6304

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting transcriptional condensates is an emerging paradigm for cancer therapy. A key player is the transcriptional coactivator YAP (Yes-associated protein), which drives tumor-specific programs that fuel tumor progression and therapeutic resistance. Cyclin K, partnered with cyclin-dependent kinases (CDKs) CDK12/CDK13, is essential for transcription elongation, but its role in specific oncogenic programs was unclear. Here, we identify Cyclin K as an essential vulnerability across multiple cancer types. The CDK12/Cyclin K complex binds YAP via Cyclin K and forms a regulatory condensate to bridge YAP phosphorylation by CDK12. Such a phosphorylation at threonine-398 impedes YAP inhibition by its canonical LATS kinases, stabilizes YAP, and enables its further condensation with TEAD4 to stimulate YAP oncogenic activity. Coexpression of CDK12/Cyclin K and YAP predicts sensitivity to Cyclin K inhibitors in hepatocellular carcinoma cells and patient-derived xenografts. Thus, we define CDK12/Cyclin K as a critical regulator of YAP-driven transcriptional addiction and a biomarker for patient stratification who mostly benefit from therapies targeting the CDK12/Cyclin K-YAP axis.

Indexed as

Adaptor Proteins, Signal TransducingCarcinoma, HepatocellularCyclin-Dependent KinasesCyclinsLiver NeoplasmsTranscription FactorsAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMicePhosphorylationYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCCNK protein, humanCDK12 protein, humanCyclin-Dependent KinasesCyclinsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID42397909
PMCPMC13330896

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.