Evidence map›Paper›PMID 32606744›Full record

ArticleOncoTargets and therapy2020

Antitumor Actions of Intratumoral Delivery of Membrane-Fused Mitochondria in a Mouse Model of Triple-Negative Breast Cancers.

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

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

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

  1. Pooled it
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  8. Article
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  12. Review
  13. Targeted Mitochondrial Delivery to Hepatocytes: A Review.Journal of clinical and translational hepatology · 2022
    Review
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  15. Article
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  17. Review
  18. Challenges in Promoting Mitochondrial Transplantation Therapy.International journal of molecular sciences · 2020
    Review
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

8 authors at 2 institutions 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 WuDepartment of Medicine, College of Medicine, China Medical University, Taichung 40447, 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-Tung ChenComprehensive Breast Cancer Center, Changhua Christian Hospital, Changhua 50094, Taiwan.
Chin-San LiuVascular and Genomic Center, Changhua Christian Hospital, Changhua 50094, Taiwan.
Changhua Christian Hospital · TWChina Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe transfer of whole mitochondria has been demonstrated to be beneficial for treating breast cancer because it induces apoptosis and drug sensitivity; however, in vivo evidence of this benefit remains scant. The present study compared the transplantation of mitochondria with instinctive (Mito) and membrane-fused morphologies induced by Pep-1 conjugation (P-Mito) using a mouse model of triple-negative breast cancers. MATERIALS AND

methodsMice with advanced severe immunodeficiency received orthotopic implantation of MDA-MB-231 human breast cancer cells followed by transplants of 5-bromo-2'-deoxyuridine (BrdU)-labeled Mito or P-Mito (200 μg [10 μg/μL]) through intratumoral injection at multiple points once a week for 4 weeks.

resultsAfter 1 month of consecutive treatment, 8.2% and 14.2% of the BrdU-labeled mitochondria were preserved in tumors of the Mito and P-Mito groups, respectively. Both Pep-1 and P-Mito treatments reduced tumor weight (21.7% ± 2.43% vs 40.6% ± 2.28%) and led to marked inhibition of Ki67 staining and angiogenesis. However, only the P-Mito group exhibited obvious necrosis and DNA fragmentation accompanied by an altered tumor microenvironment, which included reduced oxidative stress and size of cancer-associated fibroblast populations and enhanced immune cell infiltration. Transmission electron microscopy images further revealed an elongated network of perinuclear mitochondria fused with a few peripheral mitochondria in the nonnecrotic area in the P-Mito group as well as increases in mitochondrial fusion proteins and parkin compared with mitochondrial fission proteins.

conclusionIn this study, the results of mitochondrial transplantation emphasized that the facilitation of mitochondrial fusion is a critical regulator in breast cancer therapy.

Indexed as

animal model of breast cancerMDA-MB-231mitochondrial fusionmitochondrial transplantationPep-1tumor growth

Identifiers

PMID32606744
PMCPMC7294573
OpenAlexW3033978931

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.