ArticleCell death & disease2016
Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 3 of them syntheses that pooled it.
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Who cites it
112 citing papers in PubMed, 3 syntheses or guidelines pooled it, 185 citations in OpenAlex.
- Unveiling the functional paradigm of exosome-derived long non-coding RNAs (lncRNAs) in cancer: based on a narrative review and systematic review.Journal of cancer research and clinical oncology · 2023Pooled it
- The Value of Dysregulated LncRNAs on Clinicopathology and Survival in Non-Small-Cell LungFrontiers in genetics · 2022Pooled it
- The prognostic significance of long noncoding RNAs in non-small cell lung cancer: a meta-analysis.Oncotarget · 2017Pooled it
- Long noncoding RNAs at the crossroads of smoking, oxidative stress, inflammation, and lung disease.Archives of toxicology · 2026Review
- Lysine-specific histone demethylase 1a regulates nephron development and long-term transcriptional programming.JCI insight · 2026Article
- Non-coding RNAs-based Therapy and Angiogenesis: A New Era for the Management of Gliomas.Current gene therapy · 2026Review
- LncRNANon-coding RNA research · 2025Article
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- Androgen Receptor Promotes Lung Cancer Metastasis by Modifying the miR23a-3p/EPHB2 Pathway.Current medical science · 2024Article
- Long Non-Coding RNAMolecules (Basel, Switzerland) · 2024Review
- Article
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- Exosomal lncRNAs as regulators of breast cancer chemoresistance and metastasis and their potential use as biomarkers.Frontiers in oncology · 2024Review
- Emerging roles of long non-coding RNAs in osteosarcoma.Frontiers in molecular biosciences · 2024Review
- DHRS4-AS1 regulate gastric cancer apoptosis and cell proliferation by destabilizing DHX9 and inhibited the association between DHX9 and ILF3.Cancer cell international · 2023Article
- A Notch signaling-related lncRNA signature for predicting prognosis and therapeutic response in clear cell renal cell carcinoma.Scientific reports · 2023Article
- PRC2 mediated KLF2 down regulation: a therapeutic and diagnostic axis during tumor progression.Cancer cell international · 2023Review
- Jdp2 is a spatiotemporal transcriptional activator of the AhR via the Nrf2 gene battery.Inflammation and regeneration · 2023Article
- Long Non-Coding RNAs in Venous Thromboembolism: Where Do We Stand?International journal of molecular sciences · 2023Review
- EIF4A3 stabilizes the expression of lncRNA AGAP2-AS1 to activate cancer-associated fibroblasts via MyD88/NF-κb signaling.Thoracic cancer · 2023Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, long non-coding RNAs (lncRNAs) are identified as new crucial regulators of diverse cellular processes, including cell proliferation, differentiation and cancer cells metastasis. Accumulating evidence has revealed that aberrant lncRNA expression plays important roles in carcinogenesis and tumor progression. However, the expression pattern and biological function of lncRNAs in non-small-cell lung cancer (NSCLC) remain largely unknown. In this study, we performed comprehensive analysis of lncRNA expression in human NSCLC samples by using microarray data from Gene Expression Omnibus. After validation in a cohort of 80 pairs of NSCLC tissues, we identified a differentially expressed novel oncogenic lncRNA termed as AGAP2-AS1. The AGAP2-AS1 expression level was significantly upregulated in NSCLC tissues and negatively correlated with poor prognostic outcomes in patients. In vitro loss- and gain-of-function assays revealed that AGAP2-AS1 knockdown inhibited cell proliferation, migration and invasion, and induced cell apoptosis. In vivo assays also confirmed the ability of AGAP2-AS1 to promote tumor growth. Furthermore, mechanistic investigation showed that AGAP2-AS1 could bind with enhancer of zeste homolog 2 and lysine (K)-specific demethylase 1A, and recruit them to KLF2 and LATS2 promoter regions to repress their transcription. Taken together, our findings indicate that AGAP2-AS1 may act as an oncogene by repressing tumor-suppressor LATS2 and KLF2 transcription. By clarifying the AGAP2-AS1 mechanisms underlying NSCLC development and progression, these findings might promote the development of novel therapeutic strategies for this disease.
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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.