Evidence map›Paper›PMID 34001131›Full record

ArticleJournal of translational medicine2021

CCL21 activation of the MALAT1/SRSF1/mTOR axis underpins the development of gastric carcinoma.

Qianmei Fu, Xiaohong Tan, Huaming Tang, Jijiang Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. The Relationship betweenMedicina (Kaunas, Lithuania) · 2022
    Pooled it
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  10. Noncoding RNAs as sensors of tumor microenvironmental stress.Journal of experimental & clinical cancer research : CR · 2022
    Review
  11. The microRNA-202 as a Diagnostic Biomarker and a Potential Tumor Suppressor.International journal of molecular sciences · 2022
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  14. Bioinformatics Analysis Revealing the Correlation between NF-Computational and mathematical methods in medicine · 2022
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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

4 authors at 1 institution in 1 country.

Qianmei FuOncology Department, The People's Hospital of Kaizhou District, Chongqing, 405400, People's Republic of China.
Xiaohong TanOncology Department, The People's Hospital of Kaizhou District, Chongqing, 405400, People's Republic of China.
Huaming TangGeneral Surgery Department, The People's Hospital of Kaizhou District, Chongqing, 405400, People's Republic of China. 122183455@qq.com.ORCID 0000-0002-6110-4271
Jijiang LiuGeneral Surgery Department, The People's Hospital of Kaizhou District, Chongqing, 405400, People's Republic of China. 470162456@qq.com.
People's Hospital of Kaizhou District · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAs a significant cause of malignancy mortality, gastric carcinoma (GC) has been well documented to be an often-fatal diagnosis. Despite the limitations of effective therapy, immunotherapy has emerged as a promising therapeutic approach capable of killing cancer cells via the immune system. The current study was conducted to investigate the effect of cytokine C-C motif chemokine ligand 21 (CCL21) on GC progression through the metastasis-associated lung adenocarcinoma transcript 1/serine arginine-rich splicing factor 1/mammalian target of rapamycin (MALAT1/SRSF1/mTOR) axis.

methodsBioinformatics analysis was conducted to identify the key genes associated with GC and to subsequently predict their downstream genes. The effect of CCL21, MALAT1, and SRSF1 on the malignant phenotypes and epithelial-mesenchymal transition (EMT) of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo were assessed by expression determination and plasmid transfection. Additionally, RNA pull-down and RNA binding protein immunoprecipitation experiments were performed to determine the MALAT1-microRNA-202-3p (miR-203-3p) interaction and miR-202-3p-SRSF1 interaction followed by the analysis of their effect on the mTOR pathway.

resultsCCL21 was identified as a key GC immune gene. Overexpressed CCL21, MALAT1, and SRSF1 along with poorly expressed miR-202-3p were identified in the GC cells. CCL21 induced the MALAT1 expression in a time- and dose-dependent manner. Functionally, MALAT1 targeted miR-202-3p but upregulated SRSF1 and activated mTOR. Crucially, evidence was obtained indicating that CCL21 promoted both the malignant phenotypes and EMT of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo by increasing the MALAT1-induced upregulation of SRSF1.

conclusionsTaken together, the key observations of our study provide evidence that CCL21 enhances the progression of GC via the MALAT1/SRSF1/mTOR axis, providing a novel therapeutic target for the treatment of GC.

Indexed as

CarcinomaMicroRNAsRNA, Long NoncodingCell Line, TumorChemokine CCL21ChemokinesGene Expression Regulation, NeoplasticHumansLigandsSerine-Arginine Splicing FactorsStomach NeoplasmsTOR Serine-Threonine KinasesCCL21 protein, humanChemokine CCL21ChemokinesLigandsMicroRNAsMIRN202 microRNA, humanMIRN203 microRNA, humanMTOR protein, humanRNA, Long NoncodingSerine-Arginine Splicing FactorsSRSF1 protein, humanTOR Serine-Threonine KinasesC–C motif chemokine ligand 21Gastric carcinomaMammalian target of rapamycinMetastasis-associated lung adenocarcinoma transcript-1Serine arginine-rich splicing factor 1

Identifiers

PMID34001131
PMCPMC8127212
OpenAlexW3161402977

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.