ArticleProtein and peptide letters2025
Role of TPD52 in Endometrial Cancer: Impact on EMT and the PI3K/AKT and ERK/MAPK Signaling.
Article in Protein and peptide letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Diagnostic performance of systemic inflammatory and nutritional indices and their association with clinicopathological features in endometrial cancer: a retrospective study.BMC women's health · 2026Observational
- Establishiment of PANoptosis-related prognostic signature and experimental identification of SIGLEC1 as an oncogenic biomarker in endometrial cancer.Discover oncology · 2026Article
- Network toxicology and bioinformatic investigation of the association between Bisphenol A and endometrial cancer.Scientific reports · 2026Article
- miR-196b inhibits tumor proliferation and metastasis by targeting GATA6 in endometrial cancer.Biology direct · 2026Article
- PLK1/FOXM1-associated tumor-cell state and macrophage-related immune features in endometrial cancer.Frontiers in oncology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEndometrial carcinoma (EC) incidence and mortality continue to rise, and reliable therapeutic targets remain scarce. We aimed to define the oncogenic role and mechanism of tumor protein D52 (TPD52) in EC, focusing on epithelial-mesenchymal transition (EMT) and the PI3K/AKT and ERK/MAPK signaling pathways.
methodsIn this study, we assessed the expression levels of TPD52 in EC tissues and benign endometrial tissues using immunohistochemistry. To further investigate the role of TPD52, we performed experiments both
resultsTPD52 was significantly upregulated in EC tissues compared with those of benign endometrial tissues. Silencing TPD52 significantly inhibited cell proliferation, migration, and invasion, whereas TPD52 overexpression produced the opposite effects. TPD52 facilitates epithelial-mesenchymal transition (EMT). Moreover, TPD52 stimulates the PI3K/AKT and ERK/MAPK signaling pathways. DISCUSSION: These data position TPD52 as a bona fide EC oncoprotein that drives EMT via dual PI3K/AKT-ERK/MAPK signaling. Limitations include the modest patient cohort and the lack of clinical-pathological correlation analyses.
conclusionTPD52 promotes EC progression through EMT and PI3K/AKT and ERK/MAPK activation, offering a promising therapeutic target whose clinical utility warrants further investigation.
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