Evidence map›Paper›PMID 29568233›Full record

ArticleCancer cell international2018

The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma.

Bin Liu, Chun-Feng Pan, Guo-Liang Yao, Ke Wei, Yang Xia, Yi-Jiang Chen

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

Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Bin LiuDepartment of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 Jiangsu China.
Chun-Feng PanDepartment of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 Jiangsu China.
Guo-Liang YaoDepartment of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 Jiangsu China.
Ke WeiDepartment of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 Jiangsu China.
Yang XiaDepartment of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 Jiangsu China.
Yi-Jiang ChenDepartment of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029 Jiangsu China.ORCID 0000-0001-7884-4682
Jiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEsophageal squamous cell carcinoma (ESCC) is one of the prevalent and deadly cancers worldwide, especially in China. Considering the poor prognosis of ESCC, the aim of this study is to dissect the effects of long non-coding RNA (lncRNA) AK001796 on cell proliferation and cell cycle in vitro and tumorigenicity in vivo, providing therapeutic targets for ESCC.

methodsWe conducted quantitative real time PCR to detect the expression level of lncRNA AK001796 in human ESCC tumor and adjacent non-tumor tissues, and analyzed the correlation between lncRNA AK001796 expression and clinicopathologic feature of ESCC patients. Then we knocked down the expression of lncRNA AK001796 in human ESCC cell lines Eca-109 and TE-1, and next inspected cell cycle and apoptosis condition in these cells using flow cytometry. Subsequently, we used CCK-8 assay to test proliferation ability of the lncRNA AK001796-silenced ESCC cells, and the MDM2/p53 signaling pathway in these cells was analyzed by western blot analysis. At last, the ESCC xenograft models were established to verify the role of lncRNA AK001796 on the occurrence and development of ESCC.

resultsIn this study, we demonstrated that lncRNA AK001796 was significantly upregulated in ESCC tumor tissues compared to adjacent non-tumor tissues. Knockdown of lncRNA AK001796 inhibited ESCC cell growth, cell cycle, and tumor growth in a xenograft mouse model via regulating MDM2/p53 signal pathway. The expression of lncRNA AK001796 was positively correlated with MDM2 levels in human ESCC samples.

conclusionsOverall, lncRNA AK001796 regulates cell proliferation and cell cycle via modulating MDM2/p53 signaling in ESCC, which provides a new insight into the treatment targets for ESCC.

Indexed as

Esophageal squamous cell carcinomalncRNA AK001796MDM2/p53 signaling pathwayTumor growthTumorigenicity

Identifiers

PMID29568233
PMCPMC5857070
OpenAlexW2801876764

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.