ArticleMolecular and cellular biochemistry2013
Serum protein N-glycan alterations of diethylnitrosamine-induced hepatocellular carcinoma mice and their evolution after inhibition of the placental growth factor.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- MicroRNA-4491 enhances cell proliferation and inhibits cell apoptosis in non-small cell lung cancer via targeting TRIM7.Oncology letters · 2021Article
- Construction of a set of novel and robust gene expression signatures predicting prostate cancer recurrence.Molecular oncology · 2018Article
- Specific N-glycans of Hepatocellular Carcinoma Cell Surface and the Abnormal Increase of Core-α-1, 6-fucosylated Triantennary Glycan via N-acetylglucosaminyltransferases-IVa Regulation.Scientific reports · 2015Article
- Insights into glycan biosynthesis in chemically-induced hepatocellular carcinoma in rats: A glycomic analysis.World journal of gastroenterology · 2015Article
- The transcriptional profiling of glycogenes associated with hepatocellular carcinoma metastasis.PloS one · 2014Article
- Generalized portrait of cancer metabolic pathways inferred from a list of genes overexpressed in cancer.Genetics research international · 2014Article
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6 authors at 1 institution in 1 country.
Funding
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Abstract
Placental growth factor (PlGF) inhibition produced promising results in reducing tumor burden in a diethylnitrosamine (DEN)-induced mouse model for hepatocellular carcinoma (HCC). The aim of this study was to non-invasively assess the improved histology by performing a serum glycomic analysis. To elucidate the molecular mechanism underlying the observed glycomic effects, we investigated the transcription and expression of E26 transformation-specific sequence 1 (Ets-1), a transcription factor essential for the glycomic and angiogenic changes in malignant transformation, including its different phosphorylated forms that result from activation of the MAP kinase and a Ca(2+)-dependent pathway. In addition, three Ets-1-dependent glycosyltransferase genes, Mgat4a, Mgat4b, and Mgat5, were also evaluated. HCC was induced in mice by weekly injections with DEN for 16, 20, 25, and 30 w. In the treatment study, mice were injected with DEN for 25 w and subsequently treated with PlGF antibodies (5D11D4) for 5 w. Finally, PlGF-/- mice were injected with DEN for 20, 25, and 30 w. Serum N-glycans were analyzed with DNA sequencer-assisted fluorophore-assisted capillary electrophoresis and compared with histology. Maximum altered N-glycan phenotype was reached after 20 w of DEN-injections, i.e., when the first neoplastic lesions started to appear. 5D11D4-treatment improved the glycomic phenotype in that 7 of the 11 altered glycans tended to normalize. The PlGF-/- mice also showed a normalization trend, although not to the same extent of the treatment group. Number of Ets1, Mgat4a, Mgat4b, and Mgat5 transcripts increased considerably in DEN-injected mice, however, a non-significant decrease was observed after 5D11D4-treatment. On the protein level, 5D11D4-treatment had a prominent effect on the MAP kinase pathway with a significant p38 activation, yet independent of Ets-1 function.
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