ArticleMolecular medicine (Cambridge, Mass.)2024
CHRDL1 inhibits OSCC metastasis via MAPK signaling-mediated inhibition of MED29.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- IGF2BP2 Promotes Oral Squamous Cell Carcinoma Progression and Is Associated with MAPK Signaling and Macrophage-Related Immune Features.ACS omega · 2026Article
- The Mediator Complex: From Transcriptional Regulation to Disease Pathogenesis.International journal of molecular sciences · 2026Review
- C-X-C motif chemokine ligand 13 and the C-X-C motif chemokine receptor 5-c-Jun N-terminal kinase-nuclear factor kappa B-matrix metalloproteinase 9 axis in oral squamous cell carcinoma metastasis.Journal of dental sciences · 2026Article
- Serum metabolomics reveals distinctive signature of cancer staging in oral squamous cell carcinoma.BMC oral health · 2025Article
- METTL3 mediates m6A methylation modification of ULBP2 and affects the progression of cervical cancer.Hereditas · 2025Article
- Mediator-29 limits Caenorhabditis elegans fecundity.Genetics · 2025Article
- Semaglutide, a glucagon-like peptide-1 receptor agonist, inhibits oral squamous cell carcinoma growth through P38 MAPK signaling pathway.Journal of cancer research and clinical oncology · 2025Article
- Pan-cancer analysis of CHRDL1 expression and its mechanistic role in inhibiting EMT via the TGF-β pathway in lung adenocarcinoma.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundCHRDL1 belongs to a novel class of mRNA molecules. Nonetheless, the specific biological functions and underlying mechanisms of CHRDL1 in oral squamous cell carcinoma (OSCC) remain largely unexplored.
methodsRT-qPCR and immunohistochemical staining were employed to assess the mRNA and protein expression levels of the MED29 gene in clinical samples of OSCC. Additionally, RT-qPCR and Western Blot analyses were conducted to investigate the mRNA and protein expression levels of the MED29 gene specifically in OSCC. The impact of MED29 on epithelial-mesenchymal transition (EMT), invasion, and migration of OSCC was evaluated through scratch assay, transwell assay, and immunofluorescence staining. Furthermore, wound healing assay and Transwell assay were utilized to examine whether CHRDL1 influences the malignant behavior of OSCC by modulating MED29 in vitro. The regulatory role of CHRDL1 on MED29 was further elucidated in vivo through a tail vein lung metastasis model in nude mice.
resultsMED29 expression was elevated in tumor tissues of OSCC patients compared with adjacent cancer tissues. Moreover, in CAL27 and SCC25 cell lines, MED29 was upregulated and associated with increased cell migration and invasion abilities. Overexpression of MED29 facilitated EMT in OSCC cell lines, whereas knockdown of MED29 impeded EMT, resulting in diminished cell migration and invasion capacities. CHRDL1 exerted inhibitory effects on the expression of MED29, thereby suppressing EMT progression and consequently restraining the invasion and migration of OSCC cells. Furthermore, CHRDL1 mediated the inhibition of migration of OSCC cell lines to the OSCC through its regulation of MED29.
conclusionsMED29 facilitated the epithelial-mesenchymal transition process in OSCC, thereby promoting migration and invasion. On the other hand, CHRDL1 exerted inhibitory effects on the invasion and metastasis of OSCC by suppressing MED29 through the inhibition of the MAPK signaling pathway.
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