ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
MISP Suppresses Ferroptosis via MST1/2 Kinases to Facilitate YAP Activation in Non-Small Cell Lung Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Exosomal circPDSS1 Derived From Gastric Cancer Cells Promotes Natural Killer Cell Ferroptosis by Regulating the miR-142-3p/ACSL4 Molecular Axis.Applied biochemistry and biotechnology · 2026Article
- Ferroptosis: Newly Emerged Regulator for Human Disease.MedComm · 2026Review
- The dual role of the crosstalk between autophagy and ferroptosis in lung cancer treatment: Advances in mechanisms and therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- miR-495-3p promotes chronic obstructive pulmonary disease by activating ferroptosis in lung epithelial cells through regulation of the ETS1/GPX4 axis.Molecular biology reports · 2026Article
- APMAP regulated by YY1 transcription mediates ferroptosis and metastasis in non-small cell lung cancer through the PI3K/AKT/mTOR pathway.Journal of molecular histology · 2026Article
- Restoring osimertinib sensitivity in EGFR-mutant NSCLC: the role of anlotinib in modulating Wnt/β-catenin/YAP pathways.American journal of cancer research · 2026Article
- EM2, a Natural Product MST1/2 Kinase Activator, Suppresses Non-Small Cell Lung Cancer via Hippo Pathway Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting ferroptosis in lung cancer: pharmacological regulation, nanomedicine-based delivery, and AI-enabled translational strategies.American journal of cancer research · 2026Review
- Tumour Cell Size Control and Its Impact on Tumour Cell Function.Cell proliferation · 2025Review
- MISP promotes the progression of lung adenocarcinoma through Inhibition of the Hippo signaling pathway.Discover oncology · 2025Article
- The components and regulation of the Hippo pathway and its relationships with the progression and treatment of Non-small cell lung cancer (NSCLC).Cancer cell international · 2025Review
- Identification of HMOX-1-Targeting Natural Compounds inPharmaceuticals (Basel, Switzerland) · 2025Article
- MISP Suppresses Ferroptosis via MST1/2 Kinases to Facilitate YAP Activation in Non-Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multiple signaling pathways in the frontiers of lung cancer progression.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Despite advances in non-small cell lung cancer (NSCLC) therapies, resistance remains a major challenge. Ferroptosis, a form of regulated cell death, plays a key role in cancer progression and treatment response. However, the mechanisms governing ferroptosis in NSCLC are not fully understood. The Hippo pathway, which regulates cell proliferation, has recently been implicated in ferroptosis regulation. In this study, we identify Mitotic Spindle Positioning (MISP) as a critical inhibitor of ferroptosis in NSCLC. MISP is upregulated in NSCLC tissues, and its loss sensitizes cells to ferroptosis, reducing cell proliferation in vitro and in vivo. Mechanistically, MISP binds to the SARAH domain of MST1/2 kinases, inhibiting their homodimerization and autophosphorylation, leading to sustained activation of YAP, a transcriptional coactivator in the Hippo pathway. YAP activation increases SLC7A11 expression, which protects cells from ferroptosis. We also identify a mutant MISP-R390/391A that disrupts MISP-MST1/2 binding, further illustrating the MST1/2-dependent inhibition of Hippo signaling. Notably, MISP is a target of YAP, creating a feedback loop that amplifies YAP signaling. Our findings suggest a novel MISP-YAP axis regulating ferroptosis, positioning MISP as a potential therapeutic target for NSCLC, especially in cases with dysregulated YAP.
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