ArticleCancer cell international2024
PRRX1-OLR1 axis supports CAFs-mediated lung cancer progression and immune suppression.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- OLR1 promotes cell proliferation and invasion while represses apoptosis via regulating histone H3 lysine 18 lactylation‑mediated LEMD1 in papillary thyroid cancer.Oncology reports · 2026Article
- Reactive Stroma as a Transversal Prognostic Biomarker for Metastasis in Breast Cancer: Integration of Digital Histopathology and Transcriptomic Profiling.International journal of molecular sciences · 2026Article
- RNA-binding protein BICC1 promotes gastric cancer progression via the PRRX1-MAPK signaling axis.Functional & integrative genomics · 2026Article
- p300: expanding beyond acetylation to mastermind lactylation-dependent tumorigenesis.Frontiers in cell and developmental biology · 2026Review
- The tumor microenvironment in lung cancer: Heterogeneity, therapeutic resistance and emerging treatment strategies (Review).International journal of oncology · 2026Review
- OLR1 is closely related to poor prognosis and immune cell infiltration in gastric cancer.Scientific reports · 2025Article
- Exploration of efferocytosis-related genes as potential therapeutic targets in endometrial cancer.Translational cancer research · 2025Article
- Cancer-associated fibroblasts-secreted lactate promotes RNA polymerase III subunit G-mediated epithelial-mesenchymal transition in non-small cell lung cancer by increasing m6A modification of zinc finger protein 384.Journal of cell communication and signaling · 2025Article
- Effects of FAPCancer drug resistance (Alhambra, Calif.) · 2025Article
- Promotion Mechanisms of Stromal Cell-Mediated Lung Cancer Development Within Tumor Microenvironment.Cancer management and research · 2025Review
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Authors and funding
8 authors.
Funding
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Abstract
objectiveTo investigate the mechanism by which cancer-associated fibroblasts (CAFs) affect the growth and immune evasion of lung cancer cells.
methodsInitially, datasets comparing CAFs with normal fibroblasts were downloaded from the GEO dataset GSE48397. Genes with the most significant differential expression were selected and validated using clinical data. Subsequently, CAFs were isolated, and the selected genes were knocked down in CAFs. Co-culture experiments were conducted with H1299 or A549 cells to analyze changes in lung cancer cell growth, migration, and immune evasion in vitro and in vivo. To further elucidate the upstream regulatory mechanism, relevant ChIP-seq data were downloaded from the GEO database, and the regulatory relationships were validated through ChIP-qPCR and luciferase reporter assays.
resultsOLR1 was significantly overexpressed in CAFs and strongly correlated with adverse prognosis in lung cancer patients. Knockdown of OLR1 markedly inhibited CAFs' support for the growth and immune evasion of lung cancer cells in vitro and in vivo. ChIP-seq results demonstrated that PRRX1 can promote OLR1 expression by recruiting H3K27ac and H3K4me3, thereby activating CAFs. Knockdown of PRRX1 significantly inhibited CAFs' function, while further overexpression of OLR1 restored CAFs' support for lung cancer cell growth, migration, and immune evasion.
conclusionPRRX1 promotes OLR1 expression by recruiting H3K27ac and H3K4me3, activating CAFs, and thereby promoting the growth, migration, and immune evasion of lung cancer cells.
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