ArticleOncology letters2017
Endocan silencing induces programmed cell death in hepatocarcinoma.
Article in Oncology letters, 2017. 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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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Endocan Knockdown Down-Regulates the Expression of Angiogenesis-Associated Genes in Il-1ß Activated Chondrocytes.Biomolecules · 2023Article
- Endocan, a novel inflammatory marker, is upregulated in human chondrocytes stimulated with IL-1 beta.Molecular and cellular biochemistry · 2021Article
- Decreased expression of endothelial cell specific molecule-1 in lung tissue in emphysematous mice and stable COPD patients.Iranian journal of basic medical sciences · 2020Article
- Prediction and identification of novel HLA-A*0201-restricted cytotoxic T lymphocyte epitopes from endocan.Journal of inflammation (London, England) · 2020Article
- Upregulating microRNA-498 inhibits gastric cancer proliferation invasion and chemoresistance through inverse interaction of Bmi1.Cancer gene therapy · 2019Article
Corrections and comments
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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
Hepatocarcinoma is a type of high-grade malignant carcinoma identified worldwide. Its rapid development and late diagnosis prevents effective tumor resection in the majority of patients, and therefore recent studies have targeted metabolic signaling pathways and the tumor microenvironment for potential treatments. To investigate whether endocan may be a gene target for hepatocarcinoma treatment, the present study employed the following measures: MTT and Transwell assays, flow cytometry, western blotting and an mRFP-GFP-LC3 double fluorescence system. Following endocan gene silencing, cell proliferation was significantly inhibited and the number of invasive cells in the endocan siRNA-treated group was reduced compared with the control-siRNA treated-group. Furthermore, the apoptosis rate was 15% and autophagy was detected in the endocan short interfering (si)RNA-treated group compared with the control-siRNA treated-group. Using western blotting to detect NF-κB expression in the nucleus, the NF-κB expression was identified to be significantly reduced in the siRNA-treated group compared with the control groups. Endocan gene silencing inhibited hepatocarcinoma cell viability and invasion, whilst inducing apoptosis and autophagy. The results of the present study suggest that the effect of endocan gene silencing on cell survival was mediated via the NF-κB signaling pathway.
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Registered trials
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