ArticleGeneral thoracic and cardiovascular surgery2024
CircRUNX1 drives the malignant phenotypes of lung adenocarcinoma through mediating the miR-5195-3p/HMGB3 network.
Article in General thoracic and cardiovascular surgery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Dualistic Roles of High Mobility Group Box 1 in Cancer and Inflammation.Cancer medicine · 2025Review
- Cuproptosis: a novel therapeutic mechanism in lung cancer.Cancer cell international · 2025Review
- Overview of high mobility group box 3 (HMGB3] protein.Molecular genetics and genomics : MGG · 2025Review
- MiR-5195-3p predicts clinical prognosis and represses colorectal cancer progression by targeting TLR4/MyD88 signaling.Cell division · 2024Article
- Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCircular RNAs (circRNAs) are key factors in the regulation of cancer progression. However, the role of circRUNX1 in lung adenocarcinoma (LUAD) progression is unclear.
methodsThe expression levels of circRUNX1, microRNA (miR)-5195-3p, and high-mobility group protein B3 (HMGB3) were detected by quantitative real-time PCR. Cell proliferation, migration, invasion and apoptosis were analyzed by EdU staining, colony formation assay, transwell assay and flow cytometry. Protein levels were measured using western blot analysis. The interaction between miR-5195-3p and circRUNX1 or HMGB3 was verified by dual-luciferase reporter assay and RIP assay. Animal experiments were performed to investigate the role of circRUNX1 in LUAD tumorigenesis.
resultsWe found that circRUNX1 was upregulated in LUAD tumor tissues and cells. CircRUNX1 knockdown suppressed LUAD cell proliferation and metastasis, while promoted apoptosis. In terms of mechanism, we found that circRUNX1 could sponge miR-5195-3p, and miR-5195-3p inhibitor abolished the regulation of circRUNX1 knockdown on LUAD cell proliferation, metastasis and apoptosis. In addition, miR-5195-3p could target HMGB3, and HMGB3 overexpression reversed the inhibition effect of miR-5195-3p on LUAD progression. Moreover, circRUNX1 knockdown reduced LUAD tumorigenesis.
conclusionCircRUNX1 facilitated LUAD proliferation and metastasis by regulating the miR-5195-3p/HMGB3 axis, suggesting that it might be a possible therapeutic target for LUAD.
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