ArticleOncotarget2020
The role of miRNA-133b and its target gene SIRT1 in FAP-derived desmoid tumor.
Article in Oncotarget, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Relationship of MicroRNA-146a rs2910164 SNP and tobacco consumption with the susceptibility of digestive system cancer.Discover oncology · 2026Article
- The genetic puzzle of FAP: exploring novel diagnostic approaches for APC/MUTYH-negative case.Hereditary cancer in clinical practice · 2025Review
- Recent Advances and Current Management for Desmoid Tumor Associated with Familial Adenomatous Polyposis.Journal of the anus, rectum and colon · 2023Review
- The Role of Pharmacotherapeutic Agents in Children with Desmoid Tumors.Paediatric drugs · 2022Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signaling pathways have a key role in driving the uncontrolled development of familial adenomatous polyposis (FAP)- associated and sporadic desmoid tumors (DTs). The relationship between the Wnt/b-catenin signaling pathway and DTs has been extensively studied, but no reliable biomarkers able to detect their histological subtype have been identified for the accurate diagnosis. In this study we studied the differences in miRNA expression between sporadic (20 patients) and FAP-associated DTs (7 patients) using microarray confirmed by quantitative PCR (qPCR). The analysis showed 19 dysregulated miRNAs. Among them miR-133b levels were significantly lower in FAP-associated DT than in sporadic DT. Therefore, two mRNAs, associated to miR-133b and β-catenin expression, the SIRT1 and ELAVL1were analyzed. The qPCR analysis showed that SIRT1 mRNA levels were significantly up-regulated in FAP-associated DT than in sporadic DT, whereas no differences in ELAVL1 expression was observed between these two DT types. In addition, a negative correlation was observed between miR-133b and SIRT1 in FAP-associated DTs, but not in sporadic DTs. The miR-133b-SIRT1-β-catenin axis may represent a novel mechanism underlying progression of FAP-associated DT.
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