Evidence map›Paper›PMID 34330293›Full record

ArticleWorld journal of surgical oncology2021

Effect and mechanism of downregulating the long-chain noncoding RNA TM4SF1-AS1 on the proliferation, apoptosis and invasion of gastric cancer cells.

Chengzhi He, Wenjing Qi, Zhihui Wang

Open access · goldAbstract read
In one paragraph

Article in World journal of surgical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 12 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

3 authors at 2 institutions in 1 country.

Chengzhi He *Department of Gastrointestinal Surgery, Wuhan Central Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 26 Shengli Street, Jiang'an District, Wuhan, 430000, Hubei Province, China.
Wenjing Qi *Wuhan College of Arts and Sciences, Wuhan, 430345, Hubei Province, China.
Zhihui WangDepartment of Gastrointestinal Surgery, Wuhan Central Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 26 Shengli Street, Jiang'an District, Wuhan, 430000, Hubei Province, China. wvqd30@163.com.ORCID http://orcid.org/0000-0003-4258-9637
Huazhong University of Science and Technology · CNWuhan College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTo investigate long-chain noncoding TM4SF1-AS1 in gastric cancer (GC) tissues and cells.

methodsTM4SF1-AS1 in 40 GC tissues and adjacent tissues was detected and compared using real-time fluorescence quantitative PCR (qRT-PCR). TM4SF1-AS1 in MKN28 and SGC7901 GC cells was downregulated using small interfering RNA (shRNA). The cells were grouped into an interference group (shTM4SF1-AS1 group) and a control group (shControl group). MTT and Transwell tests were applied to determine the proliferation and invasion of the cells in both groups, and flow cytometry was performed to assess the apoptosis rate in the two groups. Western blotting was performed to determine changes in key proteins in cells during the epithelial-to-mesenchymal transition (EMT) and in the TM4SF1 and PI3K-AKT signalling pathways in response to the downregulation of TM4SF1-AS1.

resultsThe proliferation of MKN28 and SGC7901 in the shTM4SF1-AS1 group was significantly inhibited at 48 h and 72 h compared to that in the shControl group (all P < 0.05). In the shTM4SF1-AS1 group, the number of invaded MKN28 and SGC7901 cells was significantly lower than that in the shControl group (all P < 0.05). Apoptosis in the MKN28 and SGC7901 shTM4SF1-AS1 groups was significantly higher than that in the shControl group (all P < 0.05). Compared to those in the shControl group, levels of E-cadherin in EMT-related proteins were significantly elevated (P < 0.01), while levels of N-cadherin, Snail and Twist1 were significantly decreased (all P < 0.01). After silencing the expression of LncTM4SF1-AS1, the expression levels of TM4SF1 in the shTM4SF1-AS1 group were downregulated compared to those in the shControl group, and the p-PI3K and p-AKT proteins in the PI3K-AKT signalling pathway in the shTM4SF1-AS1 group were downregulated compared to those of the shControl group.

conclusionsTM4SF1-AS1 is upregulated in gastric cancer tissues and cells. Interfering with and downregulating its expression inhibit cancer cell proliferation, invasion and the EMT and promote apoptosis. The underlying mechanism for these effects is related to silencing the TM4SF1 and PI3K-AKT signalling pathways. TM4SF1-AS1 may be a potential therapeutic target for gastric cancer.

Indexed as

RNA, Long NoncodingStomach NeoplasmsAntigens, SurfaceApoptosisCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansNeoplasm ProteinsPhosphatidylinositol 3-KinasesPrognosisAntigens, SurfaceNeoplasm ProteinsPhosphatidylinositol 3-KinasesRNA, Long NoncodingTM4SF1 protein, humanApoptosisEMTGastric cancerInvasionPI3K-AKT signalling pathwayProliferationTM4SF1TM4SF1-AS1

Identifiers

PMID34330293
PMCPMC8325262
OpenAlexW3185027737

What OpenQuestion holds

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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.