Evidence map›Paper›PMID 30674338›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Mitochondrial transplantation regulates antitumour activity, chemoresistance and mitochondrial dynamics in breast cancer.

Jui-Chih Chang, Huei-Shin Chang, Yao-Chung Wu, Wen-Ling Cheng, Ta-Tsung Lin, Hui-Ju Chang, Shou-Jen Kuo, Shou-Tung Chen, Chin-San Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 2 pooled it
6.3field-weighted citation impact, top 3% 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

111 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

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  8. Mitochondrial geneTranslational cancer research · 2026
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51 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Jui-Chih ChangVascular and Genomic Center, Changhua Christian Hospital, Changhua, 50094, Taiwan.
Huei-Shin ChangVascular and Genomic Center, Changhua Christian Hospital, Changhua, 50094, Taiwan.
Yao-Chung WuDivision of General Surgery, Department of Surgery, Changhua Christian Hospital, Changhua, 50094, Taiwan.
Wen-Ling ChengVascular and Genomic Center, Changhua Christian Hospital, Changhua, 50094, Taiwan.
Ta-Tsung LinVascular and Genomic Center, Changhua Christian Hospital, Changhua, 50094, Taiwan.
Hui-Ju ChangVascular and Genomic Center, Changhua Christian Hospital, Changhua, 50094, Taiwan.
Shou-Jen KuoDivision of General Surgery, Department of Surgery, Changhua Christian Hospital, Changhua, 50094, Taiwan.
Shou-Tung ChenDivision of General Surgery, Department of Surgery, Changhua Christian Hospital, Changhua, 50094, Taiwan. 1886@cch.org.tw.
Chin-San LiuVascular and Genomic Center, Changhua Christian Hospital, Changhua, 50094, Taiwan. liu48111@gmail.com.
Changhua Christian Hospital · TW

Funding

National Science Council MOST 106-2314-B-371-004-National Science Council MOST 106-2314-B-371-007-
6 · The paper itself

Abstract

backgroundThe transfer of whole mitochondria that occurs during cell contact has been found to support cancer progression. However, the regulatory role of mitochondria alone is difficult to elucidate due to the complex microenvironment. Currently, mitochondrial transplantation is an available approach for restoring mitochondrial function in mitochondrial diseases but remains unclear in breast cancer. Herein, effects of mitochondrial transplantation via different approaches in breast cancer were investigated.

methodsWhole mitochondria (approximately 10.5 μg/ml) were transported into MCF-7 breast cancer cells via passive uptake or Pep-1-mediated delivery. Fresh mitochondria isolated from homeoplasmic 143B osteosarcoma cybrids containing mitochondrial DNA (mtDNA) derived from health individuals (Mito) or mtDNA with the A8344G mutation (Mito

resultsCompared with P-Mito, a small portion of Mito adhered to the cell membrane, and this was accompanied by a slightly lower fluorescent signal by foreign mitochondria in MCF-7 cells. Both transplantations induced cell apoptosis by increasing the nuclear translocation of apoptosis-inducing factor; inhibited cell growth and decreased oxidative stress in MCF-7 cells; and increased the cellular susceptibility of both the MCF-7 and MDA-MB-231 cell lines to Doxorubicin and Paclitaxel. Mitochondrial transplantation also consistently decreased Drp-1, which resulted in an enhancement of the tubular mitochondrial network, but a distinct machinery through the increase of parkin and mitochondrial fusion proteins was observed in the Mito and P-Mito groups, respectively. Furthermore, although there were no differences in energy metabolism after transplantation of normal mitochondria, metabolism was switched to the energetic and glycolytic phenotypes when the mitochondria were replaced with dysfunctional mitochondria, namely, Mito

conclusionThis study reveals the antitumour potential of mitochondrial transplantation in breast cancer via distinct regulation of mitochondrial function.

Indexed as

ApoptosisBreast NeoplasmsCell ProliferationCell SurvivalDoxorubicinDrug Resistance, NeoplasmEnergy MetabolismFemaleHumansMCF-7 CellsMitochondriaMitochondrial DynamicsOxidative StressPaclitaxelDoxorubicinPaclitaxelApoptosisApoptosis-inducing factorChemoresistanceMetabolismMitochondrial dynamicMitochondrial transplantationOxidative stressPep-1

Identifiers

PMID30674338
PMCPMC6343292
OpenAlexW2918831470

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LicenceCC BY
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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.