ArticleOncology letters2021
Knockdown of lncRNA C5orf66-AS1 inhibits osteosarcoma cell proliferation and invasion via miR-149-5p upregulation.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
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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
6 citing papers in PubMed, 6 citations in OpenAlex.
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- Roles of lncRNAs in childhood cancer: Current landscape and future perspectives.Frontiers in oncology · 2023Review
- Identification of novel key regulatory lncRNAs in gastric adenocarcinoma.BMC genomics · 2022Review
- Exosomes derived from stem cells of human deciduous exfoliated teeth inhibit angiogenesis in vivo and in vitro via the transfer of miR-100-5p and miR-1246.Stem cell research & therapy · 2022Article
- Long non-coding RNA HOTAIRincreased mechanical stimulation-induced apoptosis by regulating microRNA-221/BBC3 axis in C28/I2 cells.Bioengineered · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteosarcoma (OS) is the most common primary malignant bone tumor in the pediatric age group. Despite the various potential treatments for OS, the cure rate of patients with OS remains very low. An increasing number of long non-coding RNAs (lncRNAs) have been identified as key regulators of the progression of malignant human tumors. However, the biological functions of the lncRNA C5orf66-antisense 1 (C5orf66-AS1) in OS are yet to be fully elucidated. The present study aimed to investigate the functions and underlying mechanisms of C5orf66-AS1 in OS tissues and cell lines. Expression levels of C5orf66-AS1 and microRNA (miRNA/miR)-149-5p in tissues from patients with OS and OS cells lines were evaluated using reverse transcription quantitative (RT-q)PCR. The miRNA target interaction between C5orf66-AS1 and miR-149-5p was predicted and verified using StarBase and dual-luciferase reporter assays. Cell viability, migration, invasion and apoptosis were analyzed using Cell Counting Kit-8, Transwell assays and flow cytometry, respectively. In addition, the expression levels of migration- and apoptosis-associated proteins [matrix metalloproteinase-9 (MMP-9), Bcl-2 and Bax] were determined using western blotting and RT-qPCR. The results demonstrated that C5orf66-AS1 was significantly upregulated and miR-149-5p was significantly downregulated in OS tissues and cells (MG63 and U2OS). Bioinformatics analysis further confirmed that miR-149-5p could directly bind to C5orf66-AS1. Furthermore, it was revealed that C5orf66-AS1 negatively regulated the expression of miR-149-5p in OS cells, as confirmed by the inhibition of C5orf66-AS1 expression and miR-149-5p upregulation in cells transfected with small interfering (si RNA targeting C5orf66-AS1. In addition, C5orf66-AS1 silencing significantly inhibited the proliferation, invasion and migration of U2OS cells, and stimulated cell apoptosis. These findings were reversed using miR-149-5p inhibitor. Increased Bax expression and decreased Bcl-2 and MMP-9 expression were also observed in C5orf66-AS1-siRNA transfected U2OS cells, compared with the control group. In summary, the results from the present study indicated that C5orf66-AS1 knockdown inhibits OS cell proliferation and invasion via the upregulation of miR-149-5p. This findings may provide a promising novel target for the treatment of OS.
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