ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Loss of MNX1 Sensitizes Tumors to Cytotoxic T Cells by Degradation of PD-L1 mRNA.
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 6 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Review
- Hypoxia-induced exosomal LNCOC1 orchestrates bladder cancer progression via the YBX1/PIK3CA axis and serves as a potential liquid biopsy biomarker.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Solasonine inhibits NSCLC malignant progression by regulating SLC7A11 ubiquitination degradation and inducing ferroptosis.Respiratory research · 2026Article
- YBX1 as an adaptive RNA hub in cancer: linking state-dependent RNA regulation to tumor immunity, metabolic reprogramming, and therapy resistance.Frontiers in immunology · 2026Review
- Loss of MNX1 Sensitizes Tumors to Cytotoxic T Cells by Degradation of PD-L1 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The dual-function of HSP70 in immune response and tumor immunity: from molecular regulation to therapeutic innovations.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Immune checkpoint blockade (ICB) therapy, targeting programmed cell death ligand-1 (PD-L1)/programmed cell death protein 1 (PD-1) axis and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), has exhibited amazing clinical outcomes in various types of cancers. However, only a small portion of patients benefit from ICB therapy, indicating that the mechanism underlying immune checkpoint is still unclear. Here, it is reported that motor neuron and pancreas homeobox 1 (MNX1), a homeobox domain-containing transcription factor, contributes to the tumor immune escape. MNX1 increases PD-L1 expression in cancer cells by stabilizing PD-L1 mRNA rather than activating transcription. Mechanistically, MNX1 exists in the cytoplasm of cancer cells and interacts with Y-box binding protein 1 (YBX1), a multifunctional DNA/RNA-binding protein, to enhance the binding of YBX1 to PD-L1 mRNA. MNX1 ablation activates cytotoxic T cell-mediated anti-tumor immunity and sensitizes CTLA-4 blockade therapy. Moreover, MNX1 also facilitates tumor progression in an immune-independent manner in cancer cells. In addition, MNX1 is upregulated by its adjacent long non-coding RNA MNX1-AS1 via HECT and RLD domain containing E3 ubiquitin protein ligase 2 (HERC2). Together, these results reveal MNX1 as a novel immune checkpoint regulator with promising therapeutic potential.
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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.