ArticleCellular & molecular biology letters2022
Construction and investigation of β3GNT2-associated regulatory network in esophageal carcinoma.
Article in Cellular & molecular biology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Impacts of β-1, 3-N-acetylglucosaminyltransferases (B3GNTs) in human diseases.Molecular biology reports · 2024Review
- Article
- Pan-cancer analysis identified OAS1 as a potential prognostic biomarker for multiple tumor types.Frontiers in oncology · 2023Article
- The O-glycosylating enzyme GALNT2 acts as an oncogenic driver in non-small cell lung cancer.Cellular & molecular biology letters · 2022Article
- Article
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10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGlycosyltransferases play a crucial role in various cancers. β1, 3-N-acetylglucosaminyltransferase 2, a polylactosamine synthase, is an important member of the glycosyltransferase family. However, the biological function and regulatory mechanism of β3GNT2 in esophageal carcinoma (ESCA) is still poorly understood.
methodsThe Cancer Genome Atlas and Genotype-Tissue Expression databases were used for gene expression and prognosis analysis. Quantitative real-time PCR, Western blot, and immunohistochemistry were performed to detect the expression of β3GNT2 in ESCA cell lines and tissues. In vitro assays and xenograft tumor models were utilized to evaluate the impact of β3GNT2 on ESCA progression. The downstream effectors and upstream regulators of β3GNT2 were predicted by online software and verified by functional experiments.
resultsWe found that β3GNT2 was highly expressed in ESCA tissues and positively correlated with poor prognosis in ESCA patients. β3GNT2 expression was closely associated with the tumor size, TNM stage, and overall survival of ESCA patients. Functionally, β3GNT2 promoted ESCA cell growth, migration, and invasion in vitro, as well as tumorigenesis in vivo. Mechanistically, β3GNT2 knockdown decreased the expression of the polylactosamine on EGFR. Knockdown of β3GNT2 also inhibited the JAK/STAT signaling pathway. Meanwhile, the JAK/STAT inhibitor could partly reverse the biological effects caused by β3GNT2 overexpression. Moreover, β3GNT2 expression was positively regulated by CREB1 and negatively regulated by miR-133b. Both CREB1 and miR-133b was involved in the β3GNT2-mediated ESCA progression.
conclusionsOur study, for the first time, reveals the importance of β3GNT2 in ESCA progression and offers a potential therapeutic target for ESCA.
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