ArticleiScience2024
Intra-tumoral YAP and TAZ heterogeneity drives collective NSCLC invasion that is targeted by SUMOylation inhibitor TAK-981.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- PIN1 enhances SUMOylation of YAP1 and inhibits ferroptosis via autophagy-dependent degradation of ACSL4 in cervical cancer.Cell death discovery · 2026Article
- Salvianolic Acid A Induces Ferroptosis in Non-Small Cell Lung Cancer via the SRC/YAP/GPX4 Axis.International journal of molecular sciences · 2026Article
- Notch-1 induces M2 polarization of tumor-associated macrophages via the YAP/EZH2/FOXD1/CD47 signaling axis, thereby driving non-small cell lung cancer progression.Frontiers in medicine · 2026Article
- Metabolic programming defines oxygen-sensitive subpopulation hierarchies and patterning in collective invasion.Molecular biology of the cell · 2025Article
- Single-cell RNA-seq reveals gene expression heterogeneity in NSCLC and its link to the immune microenvironment.Discover oncology · 2025Article
- Immune regulation by the SUMO family.Nature reviews. Immunology · 2025Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Non-small cell lung cancer (NSCLC) collective invasion is supported by cooperativity of proliferative (follower) and invasive (leader) cells. H1299-isolated follower cells exhibit higher Yes-associated protein (YAP) expression, while leader cells were found to express elevated transcriptional coactivator with PDZ-binding motif (TAZ/WWTR1) expression. Suppressing TAZ (not YAP) in leader cells reduced invasion. TAZ-regulated leader cell invasion is associated with activation of the EGFR-PI3K-AKT axis. NSCLC patient samples also demonstrated heterogeneity in YAP and TAZ expression. YAP and TAZ regulate proliferation of follower and leader cells. Our results highlight the need to inhibit both YAP and TAZ to effectively target their regulation of collective invasion. We identify that the SUMOylation inhibitor TAK-981 reduces YAP and TAZ expression, decreasing tumor burden and metastasis in a murine NSCLC model. Our study reveals an intra-tumoral division of labor, driven by differential YAP and TAZ expression, which can be effectively targeted with TAK-981 for NSCLC therapy.
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Registered trials
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