ArticleJournal of experimental & clinical cancer research : CR2022
Inhibition of the mitochondrial protein Opa1 curtails breast cancer growth.
Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Roles of mitochondrial fusion and fission in breast cancer progression: a systematic review.World journal of surgical oncology · 2022Pooled it
- Cancer-associated mitochondrial homeostasis disrupted and retrograde signaling activated.Medical oncology (Northwood, London, England) · 2026Review
- Protein Expression Dynamics in Breast Cancer Cells Exposed to Nano-Encapsulated Tarin, the Taro Lectin.Pharmaceutics · 2026Article
- OMA1 protects from liver injury and tumorigenesis during aging by controlling hepatic immunogenicity.The EMBO journal · 2026Article
- Review
- Role of mitochondrial translation in modulating inflammatory disease outcome: Current knowledge and future perspectives.The Journal of biological chemistry · 2026Review
- MiR-4788 promotes NSCLC progression by targeting DLG5 to enhance mitochondrial function.Human genomics · 2026Article
- HER2-driven mammary tumorigenesis enhances bioenergetics despite reductions in mitochondrial content.eLife · 2026Article
- Identification of HSPE1 as a new actionable cancer vulnerability leads to an innovative and effective combination therapy for pancreatic ductal adenocarcinoma.Molecular cancer · 2026Article
- Review
- OPA1 as a Cancer Target: Molecular Mechanisms, Structural Insights, and Strategies for Drug Development.Antioxidants (Basel, Switzerland) · 2026Review
- Targeting mitochondria as a potential therapeutic strategy against radioresistance in cancer.Frontiers in oncology · 2026Review
- High matrix stiffness triggers the YAP-OPA1-TET1/3 loop to drive chemoresistance via enhanced nuclear-mitochondrial communication.iScience · 2025Article
- Small-molecule OPA1 inhibitors reverse mitochondrial adaptations to overcome therapy resistance in acute myeloid leukemia.Science advances · 2025Article
- Targeting mitochondrial structure and dynamics for therapeutic intervention in cancer.PLoS biology · 2025Article
- Opantimirs: A class of antagonizing microRNAs that upregulate Opa1 and improve mitochondrial and disuse myopathies.Cell reports. Medicine · 2025Article
- Metastatic breast cancer cells are selectively dependent on the mitochondrial cristae-shaping protein OPA1.Cell death & disease · 2025Article
- Small molecule OPA1 inhibitors amplify cytochrome c release and reverse cancer cells resistance to Bcl-2 inhibitors.Science advances · 2025Article
- Myeloma mesenchymal stem cells' bioenergetics afford a novel selective therapeutic target.Oncogenesis · 2025Article
- Mitochondrial Dynamics in Blood Cancer Development and Progression.Current pharmacology reports · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
backgroundMitochondrial fusion and fission proteins have been nominated as druggable targets in cancer. Whether their inhibition is efficacious in triple negative breast cancer (TNBC) that almost invariably develops chemoresistance is unknown.
methodsWe used a combination of bioinformatics analyses of cancer genomic databases, genetic and pharmacological Optic Atrophy 1 (OPA1) inhibition, mitochondrial function and morphology measurements, micro-RNA (miRNA) profiling and formal epistatic analyses to address the role of OPA1 in TNBC proliferation, migration, and invasion in vitro and in vivo.
resultsWe identified a signature of OPA1 upregulation in breast cancer that correlates with worse prognosis. Accordingly, OPA1 inhibition could reduce breast cancer cells proliferation, migration, and invasion in vitro and in vivo. Mechanistically, while OPA1 silencing did not reduce mitochondrial respiration, it increased levels of miRNAs of the 148/152 family known to inhibit tumor growth and invasiveness. Indeed, these miRNAs were epistatic to OPA1 in the regulation of TNBC cells growth and invasiveness.
conclusionsOur data show that targeted inhibition of the mitochondrial fusion protein OPA1 curtails TNBC growth and nominate OPA1 as a druggable target in TNBC.
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Registered trials
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.