ArticleJournal of experimental & clinical cancer research : CR2016
Inhibition of YAP suppresses CML cell proliferation and enhances efficacy of imatinib in vitro and in vivo.
Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Hippo-YAP/TAZ Signaling in Hematological Malignancies: Molecular Mechanisms, Pathway Crosstalk and Therapeutic Potential.Cancer management and research · 2026Review
- B cell mechanobiology in health and disease: emerging techniques and insights into therapeutic responses.FEBS letters · 2025Review
- Anticancer and cancer preventive activities of shogaol and curcumin from Zingiberaceae family plants in KG-1a leukemic stem cells.BMC complementary medicine and therapies · 2025Article
- YAP condensates are highly organized hubs.iScience · 2024Article
- Inhibition of LATS kinases reduces tumorigenicity and increases the sensitivity of human chronic myelogenous leukemia cells to imatinib.Scientific reports · 2024Article
- Review
- Automatic Multi-functional Integration Program (AMFIP) towards all-optical mechano-electrophysiology interrogation.PloS one · 2022Article
- CLP36 promotes p53 deficient sarcoma progression through suppression of atrophin-1 interacting protein-4 (AIP-4)-dependent degradation of YAP1.Theranostics · 2022Article
- Deacetylation of YAP1 Promotes the Resistance to Chemo- and Targeted Therapy in FLT3-ITDFrontiers in cell and developmental biology · 2022Article
- The Hippo signaling pathway in leukemia: function, interaction, and carcinogenesis.Cancer cell international · 2021Review
- A novel fusion circular RNA F-circBA1 derived from theBioengineered · 2021Article
- The tumor suppressor role of salvador family WW domain-containing protein 1 (SAV1): one of the key pieces of the tumor puzzle.Journal of cancer research and clinical oncology · 2021Review
- Review
- Low-Temperature Argon Plasma Regulates Skin Moisturizing and Melanogenesis-Regulating Markers through Yes-Associated Protein.International journal of molecular sciences · 2021Article
- RanBP3 Regulates Proliferation, Apoptosis and Chemosensitivity of Chronic Myeloid Leukemia CellsFrontiers in oncology · 2021Article
- Regulation of Hippo-YAP signaling by insulin-like growth factor-1 receptor in the tumorigenesis of diffuse large B-cell lymphoma.Journal of hematology & oncology · 2020Article
- Boolean model of anchorage dependence and contact inhibition points to coordinated inhibition but semi-independent induction of proliferation and migration.Computational and structural biotechnology journal · 2020Article
- BCR-ABL induces tyrosine phosphorylation of YAP leading to expression of Survivin and Cyclin D1 in chronic myeloid leukemia cells.International journal of hematology · 2019Article
- Disrupting myddosome assembly in diffuse large B‑cell lymphoma cells using the MYD88 dimerization inhibitor ST2825.Oncology reports · 2019Article
- Efficient disruption of bcr-abl gene by CRISPR RNA-guided FokI nucleases depresses the oncogenesis of chronic myeloid leukemia cells.Journal of experimental & clinical cancer research : CR · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundYes-associated protein (YAP), an essential component of Hippo pathway, was identified as an oncoprotein which participated in the progression of various malignancies. However, its role in chronic myeloid leukemia (CML) remains to be further clarified.
methodsThe expression of YAP in CML cells was determined by western blotting. Next, the effects of YAP knockdown and YAP inhibitor on CML cells were evaluated by MTT assay, flow cytometry (FCM) and Wright's staining. Moreover, K562 induced mice model was employed to further investigate the role of YAP in vivo.
resultsYAP was overexpressed in CML cells. Knockdown of YAP by si-RNA or inhibition the function of YAP using verteporfin (VP) not only inhibited the proliferation, induced the apoptosis of CML cells but also reduced the expression of YAP target genes c-myc and survivin. Additionally, VP enhanced the efficacy of imatinib (IM) in vitro and suppressed leukemogenesis in vivo.
conclusionOur results indicate that YAP may play an important role in the proliferation and leukemogenesis of CML cells. Genetic or pharmacological inhibition of YAP provides a novel treatment strategy for CML.
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