ArticleOncology letters2020
miR-1301-3p promotes the proliferation and migration of lung cancer cells via direct repression of polymerase I and transcript release factor.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- miR-1301-3p promotes invasion and migration and EMT progression in esophageal cancer by downregulating NBL1 expression.Thoracic cancer · 2023Article
- MiR-4652-5p Targets RND1 to Regulate Cell Adhesion and Promote Lung Squamous Cell Carcinoma Progression.Applied biochemistry and biotechnology · 2022Article
- Circular RNA_0078767 upregulates Kruppel-like factor 9 expression by targeting microRNA-889, thereby inhibiting the progression of osteosarcoma.Bioengineered · 2022Article
- Article
- Insulin-Like Growth Factor 2 mRNA-Binding Protein 3 and Its Related Molecules as Potential Biomarkers in Small-Cell Lung Cancer.BioMed research international · 2022Article
- Has_circ_0008583 modulates hepatocellular carcinoma progression through the miR-1301-3p/METTL3 pathway.Bioengineered · 2022Article
- Aberrant Expression of miR-1301 in Human Cancer.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant expression of microRNAs (miRNAs or miRs) is associated with a number of human diseases, including lung cancer. Although numerous differentially expressed miRNAs have been identified in lung cancer via microarray and sequencing methods, to the best of our knowledge, only a small portion of these miRNAs have been experimentally verified. In the present study, miR-1301-3p expression levels in lung tumor tissues and lung cancer cells were measured by reverse transcription-quantitative PCR (RT-qPCR) and by analyzing previously published data. Cell Counting Kit-8 and Transwell assays were used to analyze the function of miR-1301-3p in lung cancer tissues and cells. Bioinformatics analysis, RT-qPCR, western blotting and a dual-luciferase reporter assay were performed to investigate the mechanism of miR-1301-3p in lung cancer cells. It was identified that miR-1301-3p is an upregulated miRNA in lung cancer via analyzing previously published microarray and The Cancer Genome Atlas-lung squamous cell carcinoma project data, and the upregulation of miR-1301-3p was confirmed in collected clinical samples and cells. Inhibition of miR-1301-3p suppressed lung cancer cell proliferation and migration. In addition, miR-1301-3p inhibition upregulated E-cadherin, an epithelial cell maker, and downregulated vimentin, a mesenchymal cell marker. Using bioinformatics analysis, it was revealed that polymerase I and transcript release factor (PTRF) is a target of miR-1301-3p. RT-qPCR, western blotting and dual-luciferase reporter assays demonstrated that PTRF is targeted by miR-1301-3p in lung cancer cells. The rescue experiments indicated that silencing PTRF could attenuate the inhibition of cell proliferation and migration induced by miR-1301-3p inhibitor in lung cancer cells. Furthermore, a strong negative correlation between miR-1301-3p and PTRF mRNA was identified in clinical samples. In summary, the present data highlight the involvement of miR-1301-3p in the proliferation and migration of lung cancer cells, indicating that miR-1301-3p may be a promising biomarker for lung cancer.
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