ArticleBioengineered2022
Long intergenic non-protein coding RNA 115 (LINC00115) aggravates retinoblastoma progression by targeting microRNA miR-489-3p that downregulates 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2).
Article in Bioengineered, 2022. 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, 17 citations in OpenAlex.
- Orchestrating glucose metabolism: PFKFB2 as a signal-integrating conductor in homeostasis and disease.The Journal of biological chemistry · 2026Review
- Molecular Biological Research on the Pathogenic Mechanism of Retinoblastoma.Current issues in molecular biology · 2024Review
- LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling.Molecular cancer · 2024Article
- Comparative clinical significance and biological roles of PFKFB family members in oral squamous cell carcinoma.Cancer cell international · 2023Article
- Decoding the regulatory roles of non-coding RNAs in cellular metabolism and disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Long non-coding RNAs involved in retinoblastoma.Journal of cancer research and clinical oncology · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
Long non-coding RNAs (lncRNAs) are key regulators of cancer. However, the role of long intergenic non-protein coding RNA 115 (LINC00115) in the regulation of retinoblastoma (RB) has not yet been studied. The expression levels of LINC00115, microRNA (miR)-489-3p, and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2 (PFKFB2) in RB tissues or cells were detected by quantitative reverse transcription-polymerase chain reaction. The proliferation and migration of cells were detected by the cell counting kit-8 and Transwell assays. Luciferase reporter gene analysis and RNA immunoprecipitation assay were used to validate the target gene interactions predicted by starBase. A xenograft tumor experiment was conducted to validate the in vivo outcomes. The expression levels of LINC00115 and PFKFB2 in RB tissues were higher than those in normal tissues, while miR-489-3p showed the opposite trend. Silencing of LINC00115 inhibited the proliferation and migration of SO-RB50 and HXO-RB44 cells. An inhibitory or facilitated effect on RB tumorigenesis was observed following PFKFB2 silencing or miR-489-3p overexpression, respectively. Moreover, LINC00115 aggravated RB progression by targeting miR-489-3p, which downregulated PFKFB2. This finding improves our understanding of the relationship between LINC00115 and RB. Furthermore, miR-489-3p and PFKFB2 may be used as potential targets for RB prevention and treatment.
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