Evidence map›Paper›PMID 33793001›Full record

ArticleJournal of clinical laboratory analysis2021

KMT2D promotes proliferation of gastric cancer cells: evidence from ctDNA sequencing.

Qiaolian Li, Riping Wu, Fan Wu, Qiang Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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, 1 synthesis or guideline pooled it, 21 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

4 authors at 1 institution in 1 country.

Qiaolian Li *Fujian Medical University Union Hospital, Fuzhou, China.
Riping Wu *Fujian Medical University Union Hospital, Fuzhou, China.
Fan WuFujian Medical University Union Hospital, Fuzhou, China.
Qiang ChenFujian Medical University Union Hospital, Fuzhou, China.ORCID https://orcid.org/0000-0002-8717-928X
Fujian Medical University · CN

Funding

Specialized Research Fund of Fujian Provincial Department of Science and Technology 2013YZ0002-2
6 · The paper itself

Abstract

backgroundctDNA sequencing could be used for early cancer screening, prognosis prediction, and medication guidance. However, data of its application in gastric cancer are still lacking. In this study, using ctDNA sequencing, we aimed to screen the mutant genes closely associated with gastric cancer and to explore the impact of these genes on gastric cancer development.

methodsctDNA for high-throughput sequencing was obtained from gastric cancer patients, and the high-frequency mutant gene KMT2D was identified. Immunohistochemical examination was conducted to assess the expression of KMT2D in gastric cancer tissues. KMT2D knockdown was performed to establish the stably transfected gastric cancer cells. Then, CCK8, plate clone formation assay, and Transwell assay were conducted, and a subcutaneous tumor-bearing model was induced in nude mice to investigate the changes in cell proliferation and invasion capability. Transcriptome sequencing was also performed to investigate the differences in cellular gene expression.

resultsDetection of ctDNA found 113 gastric cancer-related mutations, 11 of which are the top 20 high-frequency mutations of gastric cancer recorded by COSMIC (Catalogue of Somatic Mutations in Cancer, COSMIC). They are TP53, ARID1A, CDH1, PIK3CA, KMT2C, KMT2D, APC, SPEN, CTNNB1, SETBP1, and KMT2A. The gene closely related to the clinical characteristics of the patient is KMT2D. The high-frequency mutant gene KMT2D was identified in gastric cancer tissues. The positive rate of KMT2D expression in cancer tissues was 74.3%, which was higher than that in para-carcinoma tissues (56.8%). The knockdown of KMT2D inhibited the proliferation, invasion, and tumor formation capacity of the gastric cancer cells, causing differences in the gene expression profiles, and the expression of different functional gene clusters was up- or downregulated.

conclusionThe findings of this study revealed that KMT2D could be an oncogene capable of promoting gastric cancer proliferation.

Indexed as

High-Throughput Nucleotide SequencingAgedAnimalsCell Line, TumorCell ProliferationCirculating Tumor DNADNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMaleMiceMice, Inbred BALB CMice, NudeNeoplasm InvasivenessCirculating Tumor DNADNA-Binding ProteinsKMT2D protein, humanNeoplasm ProteinsctDNAgastric cancerKMT2D

Identifiers

PMID33793001
PMCPMC8059714
OpenAlexW3144249468

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.