ArticleBulletin of experimental biology and medicine2022
The Role of Long Non-Coding RNA CCAT1 and SNHG14 in Activation of Some Protein-Coding Genes Associated with the Development of Ovarian Cancer.
Article in Bulletin of experimental biology and medicine, 2022. 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, 5 citations in OpenAlex.
- LncRNA CCAT2 role in female-related cancer progression and diagnosis: a comprehensive review.Clinical and experimental medicine · 2026Review
- The roles of the small nucleolar RNA host gene family in ovarian cancer.Cancer biology & therapy · 2025Review
- LncRNA NBR2 affects pancreatic β-cell function in type 2 diabetes mellitus by targeting miR-646.Diabetology & metabolic syndrome · 2025Article
- 7-Methylguanine With a Cyclopentane Backbone: A Bright Combination for a FIT-PNA RNA Sensor.British journal of biomedical science · 2025Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Late diagnosis of ovarian cancer is one of the most important problems in its treatment. Long non-coding RNA (lncRNA) are a poorly studied, but promising type of diagnostic biomarkers. We studied the lncRNA interactome to identify biomarkers with potential significance for molecular diagnostics of ovarian cancer. By screening the TCGA database, we identified differentially expressed lncRNA CCAT1 and SNHG14. Based on the indices of complementarity of CCAT1 and SNHG14 to the mRNA sequences, we selected 5 protein-coding genes MAPK1, c-MET, TGFB2, SNAIL1, and WNT4 associated with the epithelial-mesenchymal transition. Real-time PCR on 54 ovarian cancer samples confirmed the high expression levels of CCAT1 and SNHG14 (logFC>1.5, p<0.05). A positive correlation between the expression levels of two lncRNA and mRNA of 5 genes in 6 pairs was established. The activating effect of CCAT1 and SNHG14 on the expression of these genes can be mediated by miR-203 and miR-124.
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Registered trials
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