ArticleJournal of Cancer2022
Copy number amplification-activated long non-coding RNA LINC00662 epigenetically inhibits BIK by interacting with EZH2 to regulate tumorigenesis in non-small cell lung cancer.
Article in Journal of Cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- LDHA, BIK, and CNIH4 Are Diagnostic Markers of Endoplasmic Reticulum Stress in Lung Cancer Comorbid With Sepsis: Integrating Machine Learning and Single-Cell Analysis of Immune Signaling.Mediators of inflammation · 2026Article
- Noncoding RNAs: A Novel Frontier in Liver Cancer Research and Therapy: Implications for Precision Oncology.Sub-cellular biochemistry · 2026Review
- Long Non-Coding RNAs Contribute to Glucose Starvation-Induced Dedifferentiation in Lung Adenocarcinoma.Biomolecules · 2025Article
- The role of long non-coding RNAs in lung cancer metastasis: Molecular mechanisms, pathogenesis and clinical implications.Clinical and translational medicine · 2025Review
- Identification of BIK as an unfavorable prognostic marker and novel therapeutic target in microsatellite stable colorectal cancer harboring KRAS mutations.American journal of cancer research · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, studies have shown that lncRNAs play important roles in regulation of cancer cells proliferation, apoptosis and metastasis. Here, through systematic bioinformatics analysis and screening, we identified a long noncoding RNA LINC00662 with high copy number amplification in NSCLC. High expression of LINC00662 predicted a poorer survival. The exact sequence full-length of LINC00662 was determined by rapid amplification of cDNA ends (RACE). We also found that LINC00662 could regulate lung cancer cell proliferation both in vitro and in vivo. Mechanically, we obtained global expression profile that respond to LINC00662 knockdown through RNA-Seq analysis. And we found that LINC00662 could bind to EZH2 and recruit EZH2 to the promoter regions of BIK, regulating the level of H3K27me3 in the BIK promoter, thus epigenetically repressing BIK expression. Our results shown that lncRNA LINC00662, driven by copy number amplification, promotes tumorigenesis by EZH2/BIK cell axis, indicating that it was a potential molecular target of NSCLC.
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Registered trials
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