ReviewMolecular cancer2018
The role of YAP/TAZ activity in cancer metabolic reprogramming.
Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
What it found
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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.
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Who cites it
114 citing papers in PubMed, 219 citations in OpenAlex.
- Biomaterials for intervertebral disc regeneration: Niche reprogramming, precision therapeutics, and structural reconstruction.Bioactive materials · 2027Review
- Matrix stiffness-induced YEATS2 drives HCC progression via epigenetic activation of the TGFBR2-TAZ-AKT pathway.Cell death and differentiation · 2026Article
- The Crosstalk Between YAP/TAZ and Cancer Metabolism: From Mechanistic Insights to Drug Discovery.International journal of molecular sciences · 2026Review
- KLF5-driven TAZ-FASN signaling reprograms fatty acid metabolism to support Treg differentiation in lung cancer.Journal of translational medicine · 2026Article
- Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer.Molecular oncology · 2026Review
- From force to fate: Implications of mechanomemory in lung disease.Respiratory research · 2026Review
- Cellular mechanometabolism: stimuli and implications.EMBO reports · 2026Review
- Glycolysis-driven cancer-associated fibroblasts shape T-Cell exclusion via the CXCL16-CXCR6 Axis: a metabolic-chemokine mechanism in tumor immunity.Journal of translational medicine · 2026Review
- Research on the Hippo Pathway in Cancer.Cells · 2026Review
- Lactate and lactylation: metabolic architects of tumor progression and metastasis.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- TAZ WW Domain-Mediated Regulation of Gluconeogenesis and Tumorigenesis in Hepatocellular Carcinoma through Interaction with the Glucocorticoid Receptor.Endocrinology and metabolism (Seoul, Korea) · 2026Article
- FUT8 reprograms glycolytic metabolism to promote PKM2 lactylation and drive clear cell renal cell carcinoma progression.Cell death discovery · 2026Article
- EVA1A-Mediated Signaling Networks in Physiological and Pathological Contexts: Dual Roles in Autophagy and Apoptosis.Cell biochemistry and biophysics · 2026Review
- FAM188B promotes progression of hepatocellular carcinoma by regulating YAP/TAZ via interaction with USP10.Journal of Cancer · 2026Article
- Mechanosensitive Ion Channels: Molecular Hubs Integrating Skeletal Muscle Adaptation and Systemic Homeostasis.International journal of biological sciences · 2026Review
- Elevated CD36 drives lymph node metastasis of breast cancer by activating Hippo-YAP signaling-mediated anoikis resistance.Communications biology · 2025Article
- High matrix stiffness triggers the YAP-OPA1-TET1/3 loop to drive chemoresistance via enhanced nuclear-mitochondrial communication.iScience · 2025Article
- Article
- Post-translational modifications in hepatocellular carcinoma: mechanisms and therapeutic potential.Medical oncology (Northwood, London, England) · 2025Review
- Liver regeneration-associated hepatocellular YAP1 activation prevents colorectal cancer liver metastasis through glutamine competition.Science advances · 2025Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In contrast to normal cells, which use the aerobic oxidation of glucose as their main energy production method, cancer cells prefer to use anaerobic glycolysis to maintain their growth and survival, even under normoxic conditions. Such tumor cell metabolic reprogramming is regulated by factors such as hypoxia and the tumor microenvironment. In addition, dysregulation of certain signaling pathways also contributes to cancer metabolic reprogramming. Among them, the Hippo signaling pathway is a highly conserved tumor suppressor pathway. The core oncosuppressive kinase cascade of Hippo pathway inhibits the nuclear transcriptional co-activators YAP and TAZ, which are the downstream effectors of Hippo pathway and oncogenic factors in many solid cancers. YAP/TAZ function as key nodes of multiple signaling pathways and play multiple regulatory roles in cancer cells. However, their roles in cancer metabolic reprograming are less clear. In the present review, we examine progress in research into the regulatory mechanisms of YAP/TAZ on glucose metabolism, fatty acid metabolism, mevalonate metabolism, and glutamine metabolism in cancer cells. Determining the roles of YAP/TAZ in tumor energy metabolism, particularly in relation to the tumor microenvironment, will provide new strategies and targets for the selective therapy of metabolism-related cancers.
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Registered trials
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.