ArticleCancer science2015
ERGIC3, which is regulated by miR-203a, is a potential biomarker for non-small cell lung cancer.
Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Upregulated miR‑203a‑3p and its potential molecular mechanism in breast cancer: A study based on bioinformatics analyses and a comprehensive meta‑analysis.Molecular medicine reports · 2018Pooled it
- Article
- OAS3 is a Co-Immune Biomarker Associated With Tumour Microenvironment, Disease Staging, Prognosis, and Treatment Response in Multiple Cancer Types.Frontiers in cell and developmental biology · 2022Article
- MicroRNA-490-3p and -490-5p in carcinogenesis: Separate or the same goal?Oncology letters · 2021Review
- Parallel global profiling of plant TOR dynamics reveals a conserved role for LARP1 in translation.eLife · 2020Article
- HOXD3 targeted by miR-203a suppresses cell metastasis and angiogenesis through VEGFR in human hepatocellular carcinoma cells.Scientific reports · 2018Article
- miR-203a suppresses cell proliferation by targeting E2F transcription factor 3 in human gastric cancer.Oncology letters · 2017Article
- Identification of differential expressed PE exosomal miRNA in lung adenocarcinoma, tuberculosis, and other benign lesions.Medicine · 2017Observational
- New Insight into microRNA Functions in Cancer: Oncogene-microRNA-Tumor Suppressor Gene Network.Frontiers in molecular biosciences · 2017Review
- MicroRNA-194 modulates epithelial-mesenchymal transition in human colorectal cancer metastasis.OncoTargets and therapy · 2017Article
- MicroRNA-944 Affects Cell Growth by Targeting EPHA7 in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a previous study, we found that ERGIC3 was a novel lung cancer-related gene by screening libraries of differentially expressed genes. In this study, we developed a new murine monoclonal antibody (mAb) against ERGIC3. This avid antibody (6-C4) is well suited for immunohistochemistry, immunoblotting and solid-phase immunoassays. Furthermore, we systematically investigated expressions of ERGIC3 in a broad variety of normal human tissues and various types of tumors by immunohistochemistry. In normal human tissues, 6-C4 reacted only in some epithelial cells, such as hepatocytes, gastrointestinal epithelium, ducts and acini of the pancreas, proximal and distal tubules of the kidney, and mammary epithelial cells; however, most normal human tissues were not stained. Moreover, almost all carcinomas that originated from the epithelial cells were positive for 6-C4, whereas all sarcomas were negative. Notably, 6-C4 strongly stained non-small cell lung cancer (NSCLC) cells but did not react with normal lung tissues. Hence, ERGIC3 mAb could be used in histopathological diagnosis and cytopathological testing to detect early-stage NSCLC. We also studied the mechanisms of ERGIC3 regulation in vitro and in vivo by means of bioinformatics analysis, luciferase reporter assay, miRNA expression profiling and miRNA transfection. Results showed that miR-203a downregulation induced ERGIC3 overexpression in NSCLC cells.
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