Evidence map›Paper›PMID 25639359›Full record

ArticleJournal of cellular and molecular medicine2015

Mitochondrial proteomics with siRNA knockdown to reveal ACAT1 and MDH2 in the development of doxorubicin-resistant uterine cancer.

Yi-Wen Lo, Szu-Ting Lin, Shing-Jyh Chang, Chia-Hao Chan, Kevin W Lyu, Jo-Fan Chang, Eugenie Wong Soon May, Dai-Ying Lin, Hsiu-Chuan Chou, Hong-Lin Chan

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 12% 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, 50 citations in OpenAlex.

  1. MDH2 S246 phosphorylation protects mitochondria against hypoxia/reoxygenation injury due to acetate/lactate metabolism.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 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

10 authors at 5 institutions in 4 countries.

Yi-Wen LoDepartment of Applied Science, National Hsinchu University of Education, Hsinchu, Taiwan.
Szu-Ting Lin
Shing-Jyh Chang
Chia-Hao Chan
Kevin W Lyu
Jo-Fan Chang
Eugenie Wong Soon May
Dai-Ying Lin
Hsiu-Chuan Chou
Hong-Lin Chan
National Tsing Hua University · TWMackay Memorial Hospital · TWNational Hsinchu University of Education · TWNorthumbria University · GBUniversity of Education, Winneba · GH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are key organelles in mammary cells in responsible for a number of cellular functions including cell survival and energy metabolism. Moreover, mitochondria are one of the major targets under doxorubicin treatment. In this study, low-abundant mitochondrial proteins were enriched for proteomic analysis with the state-of-the-art two-dimensional differential gel electrophoresis (2D-DIGE) and matrix-assistant laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) strategy to compare and identify the mitochondrial protein profiling changes in response to the development of doxorubicin resistance in human uterine cancer cells. The mitochondrial proteomic results demonstrate more than fifteen hundred protein features were resolved from the equal amount pooled of three purified mitochondrial proteins and 101 differentially expressed spots were identified. In which, 39 out of these 101 identified proteins belong to mitochondrial proteins. Mitochondrial proteins such as acetyl-CoA acetyltransferase (ACAT1) and malate dehydrogenase (MDH2) have not been reported with the roles on the formation of doxorubicin resistance in our knowledge. Further studies have used RNA interference and cell viability analysis to evidence the essential roles of ACAT1 and MDH2 on their potency in the formation of doxorubicin resistance through increased cell viability and decreased cell apoptosis during doxorubicin treatment. To sum up, our current mitochondrial proteomic approaches allowed us to identify numerous proteins, including ACAT1 and MDH2, involved in various drug-resistance-forming mechanisms. Our results provide potential diagnostic markers and therapeutic candidates for the treatment of doxorubicin-resistant uterine cancer.

Indexed as

Drug Resistance, NeoplasmAcetyl-CoA C-AcetyltransferaseAntibiotics, AntineoplasticApoptosisCell Line, TumorCell SurvivalDose-Response Relationship, DrugDoxorubicinElectrophoresis, Gel, Two-DimensionalFemaleHumansImmunoblottingMalate DehydrogenaseMitochondrial ProteinsProteomeProteomicsACAT1 protein, humanAcetyl-CoA C-AcetyltransferaseAntibiotics, AntineoplasticDoxorubicinMalate DehydrogenaseMitochondrial ProteinsProteomeDIGEdoxorubicinmitochondrialresistanceuterine cancer

Identifiers

PMID25639359
PMCPMC4395189
OpenAlexW1969991243

What OpenQuestion holds

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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.