ArticleAmerican journal of translational research2021
Long noncoding RNA KCNQ1 opposite strand/antisense transcript 1 promotes osteosarcoma progression through miR-154-3p/KLF12.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Osteosarcoma in a ceRNET perspective.Journal of biomedical science · 2024Review
- Caudatin Inhibits the Proliferation, Invasion, and Glycolysis of Osteosarcoma Cells via the Wnt/Evidence-based complementary and alternative medicine : eCAM · 2022Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOsteosarcoma (OS) is a common bone cancer that usually influences children. Metastasis and recurrence are the main reasons for the poor prognosis. In this study, we investigated the functions and mechanisms of KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in OS.
methodsCell viability and proliferation were detected using the CCK-8 assay and the 5-Ethynyl-2'-deoxyuridine (EdU) assay. Wound-healing assays, transwell assay and flow cytometry were used to identify cell migration, invasion, and apoptosis, respectively. The relationship among KCNQ1OT1, miR-154-3p, and KLF12 was verified by luciferase reporter assay and restricting protein immunoprecipitation (RIP) assay. Xenograft models were established to confirm the function of KCNQ1OT1 in vivo.
resultsThe expression of KCNQ1OT1 was higher in OS than in non-tumor tissues and cells. Knockdown of KCNQ1OT1 could reduce OS cell proliferation, migration, and invasion and promoted cell death. Mechanistically, KCNQ1OT1 contributed to OS formation by acting as a competitive endogenous RNA (ceRNA) and influencing miR-154-3p expression. Furthermore, we confirmed that miR-154-3p affected KLF12 expression through binding the 3'UTR region. Finally, rescue experiments determined that KCNQ1OT1 exerted major roles in OS through the miR-154-3p/KLF12 axis.
conclusionIn conclusion, our research explains the mechanism of KCNQ1OT1 in OS progression, which could serve as a new therapeutic target.
Indexed as
Identifiers
34956453PMC8661150W4206886806What 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.