Evidence map›Paper›PMID 35163779›Full record

ArticleInternational journal of molecular sciences2022

Metabolic Reprogramming in Response to Alterations of Mitochondrial DNA and Mitochondrial Dysfunction in Gastric Adenocarcinoma.

Tzu-Ching Chang, Hui-Ting Lee, Siao-Cian Pan, Shih-Han Cho, Chieh Cheng, Liang-Hung Ou, Chia-I Lin, Chen-Sung Lin, Yau-Huei Wei

Open access · goldAbstract readComparative Study
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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  3. Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026
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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

9 authors at 4 institutions in 1 country.

Tzu-Ching ChangInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli County 350, Taiwan.
Hui-Ting LeeDivision of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Mackay Memorial Hospital, Taipei 104, Taiwan.
Siao-Cian PanCenter for Mitochondrial Medicine and Free Radical Research, Changhua Christian Hospital, Changhua City 500, Taiwan.
Shih-Han ChoSchool of Life Science, National Taiwan Normal University, Taipei 116, Taiwan.
Chieh ChengSchool of Life Science, National Taiwan Normal University, Taipei 116, Taiwan.
Liang-Hung OuSchool of Life Science, National Taiwan Normal University, Taipei 116, Taiwan.
Chia-I LinDivision of Pathology, Taipei Hospital, Ministry of Health and Welfare, New Taipei City 242, Taiwan.
Chen-Sung LinSchool of Life Science, National Taiwan Normal University, Taipei 116, Taiwan.
Yau-Huei WeiDepartment of Medicine, Mackay Medical College, New Taipei City 252, Taiwan.ORCID 0000-0002-6429-2546
National Taiwan Normal University · TWChanghua Christian Hospital · TWMackay Memorial Hospital · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We used gastric cancer cell line AGS and clinical samples to investigate the roles of mitochondrial DNA (mtDNA) alterations and mitochondrial respiratory dysfunction in gastric adenocarcinoma (GAC). A total of 131 clinical samples, including 17 normal gastric mucosa (N-GM) from overweight patients who had received sleeve gastrectomy and 57 paired non-cancerous gastric mucosae (NC-GM) and GAC from GAC patients who had undergone partial/subtotal/total gastrectomy, were recruited to examine the copy number and D310 sequences of mtDNA. The gastric cancer cell line AGS was used with knockdown (KD) mitochondrial transcription factor A (TFAM) to achieve mitochondrial dysfunction through a decrease of mtDNA copy number. Parental (PT), null-target (NT), and TFAM-KD-(A/B/C) represented the parental, control, and TFAM knocked-down AGS cells, respectively. These cells were used to compare the parameters reflecting mitochondrial biogenesis, glycolysis, and cell migration activity. The median mtDNA copy numbers of 17 N-GM, 57 NC-GM, and 57 GAC were 0.058, 0.055, and 0.045, respectively. The trend of decrease was significant (

Indexed as

AdenocarcinomaAgedAged, 80 and overCase-Control StudiesCell Line, TumorCell MovementDNA-Binding ProteinsDNA Copy Number VariationsDNA, MitochondrialFemaleGastrectomyGene Expression Regulation, NeoplasticGene Knockdown TechniquesGlycolysisHumansMaleDNA-Binding ProteinsDNA, MitochondrialMitochondrial ProteinsTFAM protein, humanTranscription Factorscopy numberD310 mutationgastric adenocarcinoma (GAC)metabolic reprogrammingmitochondrial DNA (mtDNA)mitochondrial transcription factor A (TFAM)prognosis

Identifiers

PMID35163779
PMCPMC8836428
OpenAlexW4210674381

What OpenQuestion holds

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LicenceCC BY
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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.