ArticleOncology reports2020
Long non‑coding RNA CCAT1 enhances human non‑small cell lung cancer growth through downregulation of microRNA‑218.
Article in Oncology reports, 2020. 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, 13 citations in OpenAlex.
- Long noncoding RNAs at the crossroads of smoking, oxidative stress, inflammation, and lung disease.Archives of toxicology · 2026Review
- Functional significance of miR-218 in lung cancer.Journal of cancer metastasis and treatment · 2026Article
- Tissue-Specific Tumour Suppressor and Oncogenic Activities of the Polycomb-like Protein MTF2.Genes · 2023Review
- Polymorphisms in lncRNA CCAT1 on the susceptibility of lung cancer in a Chinese northeast population: A case-control study.Cancer medicine · 2023Article
- LncRNA CCAT1 downregulation increases the radiosensitivity of non-small cell lung cancer cells.The Kaohsiung journal of medical sciences · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non‑coding RNAs (lncRNAs) have critical functions in non‑small cell lung cancer (NSCLC) growth. In the present study, we showed that lncRNA‑CCAT1 was upregulated in NSCLC tissues. High expression of lncRNA‑CCAT1 was related to tumor growth and reduced survival rate. We used short hairpin RNAs (shRNAs) to inhibit the expression of lncRNA‑CCAT1 in NSCLC cells. In vitro and in vivo results demonstrated that lncRNA‑CCAT1 knockdown suppressed tumor proliferation and induced apoptosis. Furthermore, microRNA‑218 (miR‑218) was confirmed as an effective target of lncRNA‑CCAT1 in NSCLC. B lymphoma Mo‑MLV insertion region 1 homolog (BMI‑1), which served as a downstream target of miR‑218, was also inhibited by lncRNA‑CCAT1 knockdown. In conclusion, the present study indicated that upregulation of lncRNA‑CCAT1 in NSCLC is associated with tumor malignant potential. lncRNA‑CCAT1 enhances tumor growth in NSCLC by directly inhibiting miR‑218 and indirectly increasing BMI‑1 expression.
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Registered trials
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