ArticleBiochemical genetics2023
RP11-79H23.3 Inhibits the Proliferation and Metastasis of Non-small-cell Lung Cancer Through Promoting miR-29c.
Article in Biochemical genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Risk score model with two immune infiltration-related long non-coding RNAs to predict prognosis in patients with osteosarcoma.Oncology letters · 2025Article
- Review
- MicroRNAs Can Influence Ovarian Cancer Progression by Dysregulating Integrin Activity.Cancers · 2023Review
- Non-coding RNAs in lung cancer: molecular mechanisms and clinical applications.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Evidences indicate that long non-coding RNAs (lncRNAs) are closely involved and contributed to tumorigenesis and cancer progression. As a novel lncRNA, RP11-79H23.3 was found to be an anti-oncogene in bladder cancer. However, the essential roles and functions of RP11-79H23.3 in non-small-cell lung cancer (NSCLC) remains to be elucidated. Here, loss of functional assay was applied to gain insights into the functions of RP11-79H23.3 on the proliferation and metastasis capabilities of A549 and H1299 cells. Meantime, Real-time PCR was utilized to measure RP11-79H23.3 and miR-29c expression in NSCLC tissues. Dual-luciferase reporter assay, CCK8, colony formation assay, transwell and Western blot were performed to illustrate the potential molecular basis of RP11-79H23.3 in NSCLC. RP11-79H23.3 downregulation facilitated cell proliferation, migration, and invasion of NSCLC. The result of dual-luciferase reporter assay represented a direct interaction of RP11-79H23.3 with miR-29c, which suppressed miR-29c expression that showed inversely correlation in NSCLC. Moreover, RP11-79H23.3 siRNA facilitated the progression of NSCLC partially via regulating the expression of miR-29c and the activation of Wnt/β-catenin signaling pathway. Our findings highlighted that RP11-79H23.3, served as an anti-oncogene, accelerated NSCLC progression through sequestering miR-29c, providing a promising therapeutic target for NSCLC.
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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 Socratic graph.