ArticleBlood advances2019
TAZ functions as a tumor suppressor in multiple myeloma by downregulating MYC.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 36 citations in OpenAlex.
- Unc-51 like kinase 3 (ULK3) contributes to autophagy and cell survival in multiple myeloma.Nature communications · 2026Article
- Positive TAZ-TDG feedback loop drives proneural-to-mesenchymal transition to promote glioblastoma progression.Journal of translational medicine · 2026Article
- Targeting BMP and TAZ/TEAD mechanotransduction pathways impairs acute myeloid leukemia chemoresistance.Leukemia · 2026Article
- Review
- Hippo-YAP/TAZ Signaling in Hematological Malignancies: Molecular Mechanisms, Pathway Crosstalk and Therapeutic Potential.Cancer management and research · 2026Review
- NOS1AP: a potential subtype-specific dual role as a tumor suppressor and oncogene in breast cancer subtypes.Molecular biology reports · 2025Article
- Activated Hippo Pathway is Associated with a Worse Response to Trastuzumab and Worse Survival in HER2-Positive Breast Cancer.Annals of surgical oncology · 2025Article
- Multiple Myeloma in a Patient with Birt-Hogg-Dubé Syndrome.Internal medicine (Tokyo, Japan) · 2025Article
- Posttranslational modifications of YAP/TAZ: molecular mechanisms and therapeutic opportunities.Cellular & molecular biology letters · 2025Review
- Tumors and their microenvironments: Learning from pediatric brain pathologies.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Molecular basis and therapeutic implications of binary YAPOn/YAPOff cancer classes.The Biochemical journal · 2025Review
- Molecular insights unlocking therapeutic potential for multiple myeloma and bone disease management.Journal of experimental & clinical cancer research : CR · 2024Article
- Netrin-1 and UNC5B Cooperate with Integrins to Mediate YAP-Driven Cytostasis.Cancer research communications · 2024Article
- The Hippo pathway transcription factors YAP and TAZ play HPV-type dependent roles in cervical cancer.Nature communications · 2024Article
- Che-1/miR-590-3p/TAZ axis sustains multiple myeloma disease.Leukemia · 2024Article
- LATS1 Promotes B-ALL Tumorigenesis by Regulating YAP1 Phosphorylation and Subcellular Localization.Current medical science · 2024Article
- TAZ upregulates MIR-224 to inhibit oxidative stress response in multiple myeloma.Cancer reports (Hoboken, N.J.) · 2023Article
- The new world of RNA diagnostics and therapeutics.Journal of experimental & clinical cancer research : CR · 2023Article
- New insights into the ambivalent role of YAP/TAZ in human cancers.Journal of experimental & clinical cancer research : CR · 2023Review
- YAP1 and WWTR1 expression inversely correlates with neuroendocrine markers in Merkel cell carcinoma.The Journal of clinical investigation · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple myeloma (MM) is an incurable blood cancer that is often characterized by amplification and overexpression of the MYC oncogene. Despite efforts, direct targeting of MYC is not yet possible; therefore, alternative strategies to inhibit MYC activity are necessary. TAZ is a transcriptional coactivator downstream of the Hippo-signaling pathway that functions as an oncogene in many solid tumors. However, its role in hematological malignancies is largely unexplored. Here, we show that, in contrast to solid tumors, expression of TAZ is lower in hematological malignancies, and that high expression of TAZ correlates with better patient outcomes. We further show that TAZ is hypermethylated in MM patient samples and in a panel of MM cell lines. Genetic overexpression of TAZ or pharmacological upregulation of TAZ by treatment with the demethylating agent decitabine induces apoptosis. Importantly, TAZ-induced apoptosis is independent of canonical Hippo components LATS1 or the TEA-domain family of transcription factors. Instead, RNA-sequencing analysis revealed that overexpression of TAZ represses a MYC transcriptional program and we show that increased TAZ expression correlates with decreased MYC expression in both cell-line models and patient samples. Furthermore, promoter derepression of TAZ expression sensitizes MM cell lines through a reciprocal reduction in MYC expression using additional therapeutics such as bortezomib, trichostatin A, and panobinostat. Our findings uncover an unexpected role for TAZ in MM tumorigenesis and provide a compelling rationale for exploring the therapeutic potential of upregulating TAZ expression to restore sensitivity to specific therapeutics in MM.
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