ArticleInternational journal of clinical and experimental pathology2017
Long noncoding RNA CCAT2 promotes proliferation and metastasis in non-small cell lung cancer through the Wnt pathway.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Molecular Landscape of LncRNAs in Prostate Cancer: A focus on pathways and therapeutic targets for intervention.Journal of experimental & clinical cancer research : CR · 2022Review
- Emerging roles of long non-coding RNAs in cancer.Journal of biosciences · 2019Review
- Silencing CCAT2 inhibited proliferation and invasion of epithelial ovarian carcinoma cells by regulating Wnt signaling pathway.International journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colon cancer associated transcript 2 (CCAT2), a long non-coding RNA (lncRNA), was shown to be associated with colon, ovarian and prostate cancer. Recent studies showed CCAT2 was highly expressed in various tumors, including non-small cell lung cancer (NSCLC) and probably being an independent prognostic factor of this disease. However, the physiological and biochemical mechanisms for CCAT2 with NSCLC were still unknown. In this study, we performed the analysis focused on the expression, biological functions and mechanism of CCAT2 in NSCLC and found that CCAT2 was significantly up-regulated in NSCLC tissues compared with corresponding non-cancerous tissues. Knockout of CCAT2 in NSCLC cell lines using lentivirus-mediated RNA interference significantly inhibited the proliferation and metastasis of the NSCLC cells. Most importantly, Wnt/β-catenin pathway was found to be inactivated in the NSCLC cell lines after CCAT2 knockout experiment. These results indicated that CCAT2 maybe serve as an oncogenic lncRNA that promoted proliferation and metastasis of NSCLC and activated the Wnt/β-catenin pathway.
Indexed as
Identifiers
31966650PMC6965277W3028004352What OpenQuestion holds
Registered trials
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.