ArticleNeurochemical research2020
LINC00668 Modulates SOCS5 Expression Through Competitively Sponging miR-518c-3p to Facilitate Glioma Cell Proliferation.
Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Tumor-Suppressive microRNA Therapy Inhibits Growth of Glioblastoma Multiforme Xenografts.Cancers · 2026Article
- LncRNA-associated ceRNA Network Revealing the Potential Regulatory Roles of Ferroptosis and Immune Infiltration in Osteosarcoma as well as Construction of the Prognostic Model.Current medicinal chemistry · 2025Article
- Exosomes-transferred LINC00668 Contributes to Thrombosis by Promoting NETs Formation in Inflammatory Bowel Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- LINC00668 promoted non-small lung cancer progression by miR-518c-3p/TRIP4 axis.Cancer biomarkers : section A of Disease markers · 2023Article
- SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy.Bioengineered · 2022Article
- SOCS proteins and their roles in the development of glioblastoma.Oncology letters · 2022Review
- LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis.Bioengineered · 2021Article
- The LINC01119-SOCS5 axis as a critical theranostic in triple-negative breast cancer.NPJ breast cancer · 2021Article
- LINC00668 cooperated with HuR dependent upregulation of PKN2 to facilitate gastric cancer metastasis.Cancer biology & therapy · 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
6 authors.
Funding
Abstract
Glioma is a common invasive cancer with unfavorable prognosis in patients. Long non-coding RNAs (lncRNAs) exert significant functions in carcinogenesis of various cancers including glioma. Among them, long intergenic non-coding RNA 668 (LINC00668) was reported to function as oncogene in various cancers, but its molecular mechanism in glioma has not been thoroughly researched. Our current study aimed to investigate the role and molecular mechanism of LINC00668 in glioma cells. We initially found out that LINC00668 was up-regulated in glioma cells. Through a series of function assays, LINC00668 was verified to facilitate cell proliferation and inhibit apoptosis in glioma. Then, by means of online databases, RNA pull down assay and RIP assay, we verified the binding relation between LINC00668 and miR-518c-3p. Also, the next function assays exposed that miR-518c-3p was the tumor suppressor in glioma cells. Similarly, SOCS5 (suppressor of cytokine signaling 5) was found to bind with miR-518c-3p, which repressed glioma tumorigenesis by targeting SOCS5. Moreover, rescue assays manifested that LINC00668 modulated expression of SOCS5 in a miR-518c-3p-dependent way and further regulated glioma tumorigenesis. Overall, LINC00668 modulates SOCS5 expression through competitively sponging miR-518c-3p to facilitate glioma cell proliferation.
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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.