ArticleBritish journal of cancer2018
G1P3 (IFI6), a mitochondrial localised antiapoptotic protein, promotes metastatic potential of breast cancer cells through mtROS.
Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 87 citations in OpenAlex.
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- Bioinformatics analysis of IFI6 as a novel prognostic biomarker and its correlation with immune infiltration in breast cancer.Scientific reports · 2025Article
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- STX17-DT facilitates axitinib resistance in renal cell carcinoma by inhibiting mitochondrial ROS accumulation and ferroptosis.Cell death & disease · 2025Article
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- Genomic analyses of intricate interaction of TE-lncRNA overlapping genes with miRNAs in human diseases.Genes & genomics · 2024Article
- Germline variant affecting p53β isoforms predisposes to familial cancer.Nature communications · 2024Article
- Review
- The Immune Response ofInternational journal of molecular sciences · 2024Article
- Multi-Omics Analysis Reveals the IFI6 Gene as a Prognostic Indicator and Therapeutic Target in Esophageal Cancer.International journal of molecular sciences · 2024Article
- Relationships between systemic sclerosis and atherosclerosis: screening for mitochondria-related biomarkers.Frontiers in genetics · 2024Article
- Harnessing neutrophil plasticity for HCC immunotherapy.Essays in biochemistry · 2023Review
- Article
- Identification of Gene Markers Associated with COVID-19 Severity and Recovery in Different Immune Cell Subtypes.Biology · 2023Article
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundRedox deregulations are ubiquitous in cancer cells. However, the role of mitochondrial redox deregulation in metastasis remains unclear. In breast cancer, upregulation of mitochondrial antiapoptotic protein G1P3 (IFI6) was associated with poor distance metastasis-free survival (DMFS). Therefore, we tested the hypothesis that G1P3-induced mitochondrial redox deregulation confers metastatic potentials in breast cancer cells.
methodsCell migration and invasion assays; confocal and immunofluorescence microscopy; and Illumina HumanHT-12 BeadChip to assess gene expression.
resultsConsequent to its localisation on inner-mitochondrial membrane, mtROS were higher in G1P3-expressing cells (MCF-7
conclusionsG1P3-induced mtROS have a direct role in migratory structure formation and nuclear gene expression to promote breast cancer cell metastasis. Therefore, interrupting mitochondrial functions of G1P3 may improve clinical outcomes in breast cancer patients.
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