ArticleMammalian genome : official journal of the International Mammalian Genome Society2025
FOXP2 mediates ZSCAN18 transcriptional activation to inhibit oral squamous cell carcinoma progression by blocking Hedgehog signaling.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Unraveling the molecular landscape: an overview on gene expression, epigenetic alterations, and therapeutic challenges in head and neck squamous cell carcinoma.Molecular genetics and genomics : MGG · 2026Review
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Authors and funding
2 authors.
Funding
Abstract
Zinc finger and SCAN domain-containing (ZSCAN) family members have been implicated in cancer progression. This paper was to assess the role of ZSCAN18 in oral squamous cell carcinoma (OSCC). The OSCC datasets were obtained from the GEO database, and the differentially expressed gene ZSCAN18 was screened for the next analysis. ZSCAN18 protein levels in OSCC tissues and cell lines were investigated. ZSCAN18 was manually overexpressed in OSCC cells to analyze cell proliferation, invasion, migration, and stemness. The protein level of GLI1, a marker protein of the Hedgehog pathway, was detected to determine the effect of ZSCAN18 on this signaling pathway. A mouse xenograft tumor model was constructed to observe tumor growth. Rescue experiments were designed to validate the impact of the FOXP2/ZSCAN18 axis on OSCC. ZSCAN18 was lowly expressed in OSCC and predicted poor prognoses. ZSCAN18 overexpression inhibited OSCC progression, tumor cell stemness, and the Hedgehog pathway. FOXP2, an upstream transcription factor of ZSCAN18, transcriptionally activated ZSCAN18. Rescue experiments further confirmed that FOXP2 transcriptionally activated ZSCAN18 and thus inhibited stemness and tumor growth. Collectively, FOXP2 mediates ZSCAN18 transcriptional activation to inhibit OSCC by blocking Hedgehog signaling.
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Registered trials
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