ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Enhancer Reprogramming Reveals the Tumorigenic Role of PTPRZ1 in Lung Squamous Cell Carcinoma.
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.
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.
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.
- Role of NR2F2-mediated reprogramming of endothelial cells in glioblastoma progression.iScience · 2026Article
- Single-cell analysis reveals the prognostic role of immune escape in the colorectal cancer microenvironment.Translational cancer research · 2026Article
- Identification and validation of an m1A-score model to predict outcomes and immunomodulation in lung squamous cell carcinoma by integrated analysis of single-cell and bulk RNA sequencing.Discover oncology · 2026Article
- Immune signaling as a determinant of cellular identity and tissue function.Frontiers in immunology · 2026Review
- GRHL2 contributes to the maintenance of intestinal epithelial barrier integrity during LPS-induced injury.Frontiers in immunology · 2026Article
- Enhancer Reprogramming Reveals the Tumorigenic Role of PTPRZ1 in Lung Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Lung squamous cell carcinoma (LUSC) remains a lethal malignancy with limited therapeutic advancements, underscoring the need to identify novel oncogenic drivers. This study integrates multi-omics analyses-including ChIP-seq, bulk RNA-seq, single-cell ATAC/RNA-seq, and spatial transcriptomics-to delineate enhancer-driven transcriptional networks in 59 matched LUSC tumors and adjacent normal tissues. The analyses identify 3,447 tumor-specific oncogenic enhancers (SOEs) enriched for master transcription factors (SOX2, TP63, KLF5, GRHL2) that orchestrate malignant programs. Single-cell epigenomic profiling reveals these SOEs to be exclusively active in a cancer cell-like cluster, pinpointing PTPRZ1, a receptor tyrosine phosphatase, as a top SOE-driven candidate. Functional studies demonstrate that PTPRZ1 is essential for LUSC-tumorigenesis and tumor cells proliferation and migration in vitro and in vivo. Spatial transcriptomic analysis further implicates midkine (MDK) as the ligand activating PTPRZ1 in LUSC tumor tissue. Mechanistically, PTPRZ1 mediates MDK-induced PI3K phosphorylation that is essential for LUSC tumor growth. This work illustrates enhancer addiction as a hallmark of LUSC, identifies the PTPRZ1-MDK axis as an important targetable pathway, and establishes a paradigm for dissecting epigenetic vulnerabilities in solid tumors through multi-omics integration. These findings advance precision oncology strategies for LUSC, bridging epigenomic dysregulation to therapeutic intervention.
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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.