Evidence map›Paper›PMID 29298720›Full record

ArticleBiological research2018

CCAT2 is an oncogenic long non-coding RNA in pancreatic ductal adenocarcinoma.

Yi Cai, Xiaomei Li, Peng Shen, Dong Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biological research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. BRCA-mutant pancreatic ductal adenocarcinoma.British journal of cancer · 2021
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Observational
  13. Article
  14. A Review of Pancreatic Cancer: Epidemiology, Genetics, Screening, and Management.Open access Macedonian journal of medical sciences · 2019
    Review
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yi CaiDepartment of Geriatric Oncology, The General Hospital of Chinese People's Liberation Army, 28 Fuxing Road, Haidian District, Beijing, 100853, People's Republic of China.
Xiaomei LiDepartment of Geriatric Oncology, The General Hospital of Chinese People's Liberation Army, 28 Fuxing Road, Haidian District, Beijing, 100853, People's Republic of China.
Peng ShenThe Fourth Division of Department of Internal Medicine, Huailai County Hospital, Fuqianddong Rd, Huailai, Zhangjiakou, Beihe, 075400, People's Republic of China.
Dong ZhangDepartment of Geriatric Oncology, The General Hospital of Chinese People's Liberation Army, 28 Fuxing Road, Haidian District, Beijing, 100853, People's Republic of China. zhangdong_301@163.com.
Chinese People's Liberation Army · CN

Funding

Clinical Research Support Foundation of General Hospital of Chinese People's Liberation Army No.: 2015FC-TSYS-2015
6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is highly aggressive with poor prognosis. Long non-coding RNAs (lncRNAs), a group of non-coding RNAs, play important roles in the progression of PDAC. This study aimed to investigate the potential involvement of lncRNA CCAT2 in PDAC tumorigenesis.

methodsExpression of CCAT2 was detected by quantitative real-time PCR (qRT-PCR) in 80 human PDAC tissues and three PDAC cell lines. The effects of CCAT2 silencing in PANC-1 cells on cell proliferation and invasion were studied using MTT assay and transwell assay, respectively. The effect of CCAT2 silencing on tumorigenesis was assessed by PANC-1 xenograft in vivo. Using si-KRAS, the role of KRAS to regulate CCAT2 was evaluated by qRT-PCR and luciferase reporter assay. The involvement of MEK/ERK and PI3K/AKT signaling in CCAT2 regulation was investigated by pathway inhibitors PD98059 and LY294002, respectively.

resultsCCAT2 was significantly elevated in high-grade PDAC tissues and higher CCAT2 expression was correlated with lower survival rate in PDAC patients. CCAT2 was up-regulated in PDAC cell lines, as compared with normal pancreatic cells. Silencing of CCAT2 inhibited cell proliferation and invasion in PANC-1 cells in vitro, and attenuated tumorigenesis of PANC-1 xenograft in vivo. Furthermore, CCAT2 was regulated by KRAS through MEK/ERK signaling pathway.

conclusionsCCAT2 is an oncogenic lncRNA in PDAC likely regulated by the KRAS-MEK/ERK pathway. It could be a potential diagnostic biomarker and therapeutic target for PDAC.

Indexed as

Carcinoma, Pancreatic DuctalFemaleHumansMaleMiddle AgedMutationNeoplasm StagingPrognosisProto-Oncogene Proteins p21(ras)Real-Time Polymerase Chain ReactionRNA, Long NoncodingKRAS protein, humanlong non-coding RNA CCAT2, humanProto-Oncogene Proteins p21(ras)RNA, Long NoncodingKRASlncRNA CCAT2MAPK signalingPDAC

Identifiers

PMID29298720
PMCPMC5751927
OpenAlexW2782448538

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.