ArticleBioengineered2022
N6-methyladenosine-induced SVIL antisense RNA 1 restrains lung adenocarcinoma cell proliferation by destabilizing E2F1.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Overview of the interplay between m6A methylation modification and non-coding RNA and their impact on tumor cells.Translational cancer research · 2024Review
- Emerging role of RNA modification and long noncoding RNA interaction in cancer.Cancer gene therapy · 2024Review
- Article
- Establishment, characterization, and genetic profiling of patient-derived osteosarcoma cells from a patient with retinoblastoma.Scientific reports · 2024Article
- Current concepts of the crosstalk between lncRNA and E2F1: shedding light on the cancer therapy.Frontiers in pharmacology · 2024Review
- Engineered exosomes transporting the lncRNA, SVIL-AS1, inhibit the progression of lung cancer via targeting miR-21-5p.American journal of cancer research · 2024Article
- The long non-coding RNA TAZ-AS202 promotes lung cancer progression via regulation of the E2F1 transcription factor and activation of Ephrin signaling.Cell death & disease · 2023Article
- The critical roles of m6A RNA methylation in lung cancer: from mechanism to prognosis and therapy.British journal of cancer · 2023Review
- Novel insights into mutual regulation between NCancer cell international · 2023Review
- Novel insights into the multifaceted roles of mBiomarker research · 2023Review
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Authors and funding
4 authors.
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Abstract
Accumulating evidence indicates that N6-methyladenosine (m6A) and long noncoding RNAs (lncRNAs) play crucial roles in cancer development. However, the biological roles of m6A and lncRNAs in lung cancer tumorigenesis are largely unknown. In this study, SVIL antisense RNA 1 (SVIL-AS1) was downregulated in lung adenocarcinoma (LUAD) tissues and was associated with a favorable prognosis in patients with LUAD. SVIL-AS1 overexpression suppressed LUAD cell proliferation and blocked cell cycle arrest. Mechanistically, METTL3 increased the m6A modification and transcript stability of SVIL-AS1. The enhanced SVIL-AS1 expression mediated by METTL3 suppressed E2F1 and E2F1-target genes. Moreover, SVIL-AS1 accelerated E2F1 degradation. The reduction in cell proliferation induced by SVIL-AS1 overexpression could be rescued by E2F1 overexpression or METTL3 knockdown. In conclusion, our work demonstrated the role and mechanism of METTL3-induced SVIL-AS1 in LUAD, which connects m6A and lncRNA in lung cancer carcinogenesis.
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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.