ArticleCancer medicine2022
Long noncoding RNASEH1-AS1 exacerbates the progression of non-small cell lung cancer by acting as a ceRNA to regulate microRNA-516a-5p/FOXK1 and thereby activating the Wnt/β-catenin signaling pathway.
Article in Cancer medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- FOXK1: a multifaceted regulator in metabolic reprogramming and disease progression.Biology direct · 2026Review
- The role of Wnt/β-catenin signaling in lung cancer progression and therapy: a comprehensive review.Medical oncology (Northwood, London, England) · 2025Review
- circ-ATAD1 as Competing Endogenous RNA for miR-191-5p Forces Non-small Cell Lung Cancer Progression.Applied biochemistry and biotechnology · 2024Article
- Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer.Journal of translational medicine · 2024Review
- Comprehensive analysis identifies long non-coding RNA RNASEH1-AS1 as a potential prognostic biomarker and oncogenic target in hepatocellular carcinoma.American journal of cancer research · 2024Article
- RP11-79H23.3 Inhibits the Proliferation and Metastasis of Non-small-cell Lung Cancer Through Promoting miR-29c.Biochemical genetics · 2023Article
- Vitamin A- and D-Deficient Diets Disrupt Intestinal Antimicrobial Peptide Defense Involving Wnt and STAT5 Signaling Pathways in Mice.Nutrients · 2023Article
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundTill now, no study has focused on the functions of RNASEH1 antisense RNA 1 (RNASEH1-AS1) in non-small cell lung cancer (NSCLC). Accordingly, we measured the expression of RNASEH1-AS1 in NSCLC and characterized its functions in detail. Finally, our research elucidated the mechanisms that occurred downstream of RNASEH1-AS1.
methodsRNASEH1-AS1 expression was examined utilizing TCGA database and qRT-PCR. Functional experiments were conducted to study the tumor-associated functions of RNASEH1-AS1. The targeting relationship among RNASEH1-AS1, microRNA-516a-5p (miR-516a-5p), and forkhead box K1 (FOXK1) was revealed utilizing RNA immunoprecipitation and luciferase reporter assays.
resultsUtilizing TCGA database and our own cohort, we found a significantly increased level of RNASEH1-AS1 in NSCLC. The high level of RNASEH1-AS1 was markedly related with poor clinical outcomes. Knockdown of RNASEH1-AS1 expression inhibited NSCLC cell growth, metastatic capacities, and epithelial-mesenchymal transition and promoted the apoptosis in vitro, whereas RNASEH1-AS1 overexpression exerted the opposite effects. Additionally, knocking down RNASEH1-AS1 expression suppressed tumor growth in vivo. RNASEH1-AS1 was confirmed to act as a miR-516a-5p sponge, consequently upregulating FOXK1 expression in NSCLC cells. As revealed by the subsequent rescue experiments, the miR-516a-5p/FOXK1 axis served as a downstream effector of RNASEH1-AS1. In addition, by controlling the miR-516a-5p/FOXK1 axis, RNASEH1-AS1 was capable of activating the Wnt/β-catenin pathway.
conclusionRNASEH1-AS1 exacerbated the oncogenicity of NSCLC by affecting the miR-516a-5p/FOXK1 axis and consequently promoting the activation of Wnt/β-catenin pathway. Our newly identified RNASEH1-AS1/miR-516a-5p/FOXK1/Wnt/β-catenin network may offer an interesting foundation for NSCLC treatment in the clinic.
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