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| http://dx.doi.org/10.1016/j.jhep.2025.07.009 | DOI Listing |
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Integrative High-Throughput RNAi Screening Identifies BRSK1, STK32C and STK40 as Novel Activators of YAP/TAZ.
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Department of Biochemistry, Donnelly Centre, University of Toronto, Toronto, ON M5S 3E1, Canada.
Disruption of the Hippo pathway leads to activation of the YAP/TAZ transcriptional program which promotes tumor initiation, progression and metastasis in diverse cancers. Aggressive triple-negative breast cancers (TNBC) lack an effective therapy; thus, inactivating YAP and TAZ has emerged as an attractive approach and a new treatment modality. Thus, we performed two complementary high-throughput RNAi-based kinome screens to uncover cancer-associated activators of YAP/TAZ in two TNBC cell lines, MDA-MB231 and MDA-MB468.
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July 2025
Hepatology Laboratory, Solid Tumors Program, CIMA, CCUN, University of Navarra, Pamplona, Spain; Instituto de Investigaciones Sanitarias de Navarra IdiSNA, Pamplona, Spain; CIBERehd, Instituto de Salud Carlos III, Madrid, Spain. Electronic address:
Steatotic liver disease induces YAP/TAZ-driven cell competition that can suppress tumor initiation.
J Hepatol
June 2025
VIB Center for Cancer Biology; KU Leuven Department of Oncology, KU Leuven, Belgium. Electronic address:
Background & Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), are leading risk factors for liver cancer. While inflammation and fibrosis are known to promote tumorigenesis in advanced MASH, it remains unclear how earlier stages of MASLD contribute to cancer initiation. Here, we investigated how steatosis alone, in the absence of significant fibrosis and inflammation, influences liver cancer development in mouse models.
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YAP and TAZ are transcriptional co-activators that are inhibited by sequestration in the cytoplasm. Cellular signalling pathways integrate soluble, mechanical (cytoskeleton, adhesion), and geometric (cell size, morphology) cues to regulate the translocation of YAP/TAZ to the nucleus. In triple-negative breast cancer (TNBC) cells, both signalling and morphogenesis are frequently rewired, leading to increased YAP/TAZ translocation, which drives proliferation, invasion, and drug resistance.
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Department of Pharmacology and Cancer Biology, Duke University, Durham, North Carolina.
Cancer cells exploit a mesenchymal-like transcriptional state (MLS) to survive drug treatments. Although the MLS is well characterized, few therapeutic vulnerabilities targeting this program have been identified. In this study, we systematically identify the dependency network of mesenchymal-like cancers through an analysis of gene essentiality scores in ∼800 cancer cell lines, nominating a poorly studied kinase, PKN2, as a top therapeutic target of the MLS.
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