ArticleOncology research2017
Highly Expressed Antisense Noncoding RNA in the INK4 Locus Promotes Growth and Invasion of Renal Clear Carcinoma Cells via the β-Catenin Pathway.
Article in Oncology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Circulating expression and clinical significance of LncRNA ANRIL in diabetic kidney disease.Molecular biology reports · 2022Article
- Overexpressed lncRNA FTX promotes the cell viability, proliferation, migration and invasion of renal cell carcinoma via FTX/miR‑4429/UBE2C axis.Oncology reports · 2022Article
- Non-Coding RNAs in Kidney Diseases: The Long and Short of Them.International journal of molecular sciences · 2021Review
- LncRNA CDKN2B-AS1 stabilized by IGF2BP3 drives the malignancy of renal clear cell carcinoma through epigenetically activating NUF2 transcription.Cell death & disease · 2021Article
- Long noncoding RNAs as tumorigenic factors and therapeutic targets for renal cell carcinoma.Cancer cell international · 2021Review
- Upregulation of SOX2-activated lncRNA ANRIL promotes nasopharyngeal carcinoma cell growth.Scientific reports · 2018Article
Corrections and comments
- Retraction · 2022-01-28Concerns/Issues about Image ·
- Retracted
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) is involved in several human cancers. However, the role of ANRIL in renal cell carcinoma (RCC) remains unclear. This study aimed to explore whether, and how, ANRIL affects the progression of RCC. First, the expression of ANRIL in clinical tumor tissues and four kinds of RCC cell lines was evaluated. After transfection, cell viability, colony number, apoptosis, migration, and invasion were assessed. The expression of proteins related to apoptosis, epithelial-to-mesenchymal transition (EMT), and the β-catenin signaling pathway was then assessed. In addition, the effect of IWR-endo (β-catenin inhibitor) on cell viability, migration, and invasion, as well as β-catenin expression, was also evaluated. The results showed that ANRIL was highly expressed in RCC tissues and RCC cell lines. ANRIL significantly promoted cell proliferation, migration, invasion, and EMT but inhibited cell apoptosis. Additionally, the expression levels of β-catenin, Ki-67, glycogen synthase kinase 3β (GSK-3β), phosphorylated GSK-3β, T-cell transcription factor 4 (TCF-4), and leukemia enhancer factor 1 (LEF-1) were all markedly upregulated by ANRIL. The effect of ARNIL silencing was opposite to that of ANRIL overexpression. The effect of ARNIL on proliferation, migration, and invasion of RCC cells was found to be reversed by IWR-endo. In conclusion, ANRIL, which is highly expressed in RCC, acted as a carcinogen in RCC cells through the activation of the β-catenin pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.