AI Article Synopsis
- CHRDL1 is a newly identified mRNA that potentially influences oral squamous cell carcinoma (OSCC), but its specific functions and mechanisms are still unclear.
- Research utilized various techniques like RT-qPCR and immunohistochemistry to examine how the MED29 gene expression relates to OSCC progression and cellular behaviors like migration and invasion.
- Results showed that increased MED29 levels in tumor tissues promote epithelial-mesenchymal transition (EMT) and cancer cell movement, while CHRDL1 suppresses MED29, thus inhibiting OSCC cell invasion and metastasis.
Article Abstract
Background: CHRDL1 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.
Methods: RT-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.
Results: MED29 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.
Conclusions: MED29 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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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11512478 | PMC |
| http://dx.doi.org/10.1186/s10020-024-00956-y | DOI Listing |
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