ArticleCell death & disease2025
Olfactory receptor OR51B5 suppressed esophageal cancer progression through activates Calcium / N-Ras signaling.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Sphingosine‑1‑phosphate receptor 1 enhances olfactory receptor 51E1‑mediated inhibition of proliferation via Src/JNK signaling in prostate cancer cells.Oncology reports · 2026Article
- Investigating the impact of Sprouty-related EVH1 domain-containing protein 3 on gastric cancer prognosis and tumor microenvironments.Frontiers in oncology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The transcriptional regulation of olfactory receptors (ORs) plays a critical role in various biological processes, and has recently been considered a potential therapeutic target for cancer treatment. Esophageal cancer (EC) is a highly invasive neoplasm with dismal prognosis, but the specific roles of ORs in EC remain largely unexplored. Here, we developed a comprehensive workflow to identify potential functional olfactory receptor family 51 subfamily B member 5 (OR51B5) and demonstrated that OR51B5 locus acted as a key spatial element contributing to the progression of esophageal cancer. Moreover, we showed that the CTCF-EZH2 enhanced the trimethylation of lysine 27 of histone H3 (H3K27me3) and increased repressive and closed chromatin state at the OR51B5 promoter region. Subsequently we demonstrated that closed chromatin impaired the entry of RNA polymerase II and inhibited the transcription of OR51B5, thereby causing N-Ras activation and promoting tumor cell proliferation and metastasis. Our study provides an alternative workflow for discovering critical regulatory sites for control tumorigenesis, and reveals a novel OR51B5 triggering mechanism underlying esophageal cancer progression.
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Registered trials
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