ArticleJournal of applied oral science : revista FOB2025
Study of the role of transmembrane emp24 domain-containing protein 2 in oral squamous cell carcinoma.
Article in Journal of applied oral science : revista FOB, 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.
- Pan-cancer analysis of TMED2: unraveling potential immune characteristics and prognostic value in cancer therapy.Frontiers in immunology · 2025Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to investigate the role of transmembrane emp24 domain-containing protein 2 (TMED2) in oral squamous cell carcinoma (OSCC). METHODOLOGY: A bioinformatics analysis was first conducted to explore TMED2 expression in OSCC and its relation with overall survival. The analysis results were further verified by assessing TMED2 expression levels in human normal oral keratinocyte cells and human OSCC cell lines using quantitative real-time polymerase chain reaction and the Western blot. Finally, the effects of TMED2 knockdown and overexpression on the expression levels of TMED2, ADP-ribosylation factor 1, extracellular signal-regulated kinase ½, and phospho-extracellular signal-regulated kinase ½ proteins were examined in cells using the Western blot.
resultsThe GEPIA2 database showed that OSCC tissues expressed more TMED2 than normal tissues. At the cellular level, TMED2 expression significantly increased in SCC-4, HSC-3, and CAL-27 cells than in human normal oral keratinocyte cells. TMED2 knockdown reduced cell proliferation, increased the apoptosis rate in SCC-4 cells, and led to a higher proportion of cells in the G0/G1 phase and a lower proportion in the S phase.
conclusionTMED2 may promote OSCC cell proliferation and inhibit apoptosis, potentially by activation of the ADP-ribosylation factor 1/ extracellular signal-regulated kinase ½ signaling pathway.
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