ArticleFrontiers in oncology2020
Silencing of Long Non-Coding RNA LINC00607 Prevents Tumor Proliferation of Osteosarcoma by Acting as a Sponge of miR-607 to Downregulate E2F6.
Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Elevated E2F6 Expression in Colorectal Cancer Tissues and Its Association With Clinicopathological Features.World journal of oncology · 2026Article
- Long non-coding RNA LINC00607 epigenetically regulates endothelial TSPAN18 to promote hypoxia-induced thromboinflammation.The Journal of biological chemistry · 2026Article
- Epithelial-Mesenchymal Transition in Osteosarcoma as a Key Driver of Pulmonary Metastasis.Cancers · 2025Review
- Deciphering the roles of non-coding RNAs in liposarcoma development: Challenges and opportunities for translational therapeutic advances.Non-coding RNA research · 2025Review
- Role of long noncoding RNAs in the regulation of epithelial‑mesenchymal transition in osteosarcoma (Review).Oncology reports · 2025Review
- Transcriptomic analysis reveals regulation of adipogenesis via long non-coding RNA, alternative splicing, and alternative polyadenylation.Scientific reports · 2024Article
- The crosstalk between non-coding RNAs and cell-cycle events: A new frontier in cancer therapy.Molecular therapy. Oncology · 2024Review
- Circular RNA circ_0101675 Promotes NSCLC Cell Proliferation, Migration, Invasion, Angiogenesis and Immune Evasion by Sponging miR-607/PDL1 Axis.Biochemical genetics · 2024Article
- Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis.Journal of orthopaedic surgery and research · 2023Article
- The endothelial-enriched lncRNA LINC00607 mediates angiogenic function.Basic research in cardiology · 2023Article
- Overexpression of LINC00607 inhibits cell growth and aggressiveness by regulating the miR-1289/EFNA5 axis in non-small-cell lung cancer.Open medicine (Warsaw, Poland) · 2023Article
- [Overexpression of miR-607 inhibits hepatocellular carcinoma cell growth and metastasis by down-regulating TRPC5].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- Circular RNA hsa_circ_0003823 promotes the Tumor Progression, Metastasis and Apatinib Resistance of Esophageal Squamous Cell Carcinoma by miR-607/CRISP3 Axis.International journal of biological sciences · 2022Article
- Vascular Regulation by Super Enhancer-Derived LINC00607.Frontiers in cardiovascular medicine · 2022Article
- Article
- Tumor Mutation Burden-Associated LINC00638/miR-4732-3p/ULBP1 Axis Promotes Immune EscapeFrontiers in oncology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma (OS), a type of malignant bone tumor, is commonly found in children and adolescents. Although previous studies have identified that long non-coding RNAs (lncRNAs) regulate OS, it is unclear whether lncRNAs impact the progression of OS. Here, we identified
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Identifiers
What OpenQuestion holds
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.