ArticleJournal for immunotherapy of cancer2022
ELK3 modulates the antitumor efficacy of natural killer cells against triple negative breast cancer by regulating mitochondrial dynamics.
Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- ETS transcription factor ELK3: Molecular insights and translational horizons in cancer (Review).Oncology letters · 2026Review
- Strategies for Targeting Mitochondria in the Treatment of Breast Cancer.ACS pharmacology & translational science · 2026Review
- A baseline systemic inflammatory signature predicts anti-PD-1 response in advanced melanoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Synergistic immunotherapeutic effects of irreversible electroporation and CAR-NK cell therapy against hepatocellular carcinoma.Signal transduction and targeted therapy · 2026Article
- Single-cell RNA sequencing analysis revealed a potential association between ELK3 expression and the progression of multiple myeloma.Frontiers in immunology · 2026Article
- Decoding the tumor microenvironment of triple-negative breast cancer: from immune evasion to precision immunotherapy.Frontiers in immunology · 2026Review
- TMB as a predictive biomarker for ICI response in TNBC: current evidence and future directions for augmented anti-tumor responses.Clinical and experimental medicine · 2025Review
- Decoding the mechanisms underlying breast cancer brain metastasis: paving the way for precision therapeutics.Biomarker research · 2025Review
- Clinical, immune cell, and genetic features predicting survival and long-term response to first-line chemo-immunotherapy treatment for non-small cell lung cancer.Cancer immunology, immunotherapy : CII · 2025Article
- ELK3-CYFIP2 axis-mediated actin remodeling modulates metastasis and natural killer cell responses in triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Unraveling the breast cancer tumor microenvironment: crucial factors influencing natural killer cell function and therapeutic strategies.International journal of biological sciences · 2025Review
- Longitudinal multiomics analysis of aggressive pituitary neuroendocrine tumors: comparing primary and recurrent tumors from the same patient, reveals genomic stability and heterogeneous transcriptomic profiles with alterations in metabolic pathways.Acta neuropathologica communications · 2024Article
- Early Progression of Abdominal Aortic Aneurysm is Decelerated by Improved Endothelial Barrier Function via ALDH2-LIN28B-ELK3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Mitochondrial dynamics in health and disease: mechanisms and potential targets.Signal transduction and targeted therapy · 2023Review
- Role of mitochondrial alterations in human cancer progression and cancer immunity.Journal of biomedical science · 2023Review
- The ELK3-DRP1 axis determines the chemosensitivity of triple-negative breast cancer cells to CDDP by regulating mitochondrial dynamics.Cell death discovery · 2023Article
- ELK3-CXCL16 axis determines natural killer cell cytotoxicity via the chemotactic activity of CXCL16 in triple negative breast cancer.Oncoimmunology · 2023Article
- Overcoming the challenges in translational development of natural killer cell therapeutics: An opinion paper.Frontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple negative breast cancer (TNBC) is the most lethal subtype of breast cancer due to its aggressive behavior and frequent development of resistance to chemotherapy. Although natural killer (NK) cell-based immunotherapy is a promising strategy for overcoming barriers to cancer treatment, the therapeutic efficacy of NK cells against TNBC is below expectations. E26 transformation-specific transcription factor ELK3 (ELK3) is highly expressed in TNBCs and functions as a master regulator of the epithelial-mesenchymal transition.
methodsTwo representative human TNBC cell lines, MDA-MB231 and Hs578T, were exposed to ELK3-targeting shRNA or an ELK3-expressing plasmid to modulate ELK3 expression. The downstream target genes of ELK3 were identified using a combined approach comprising gene expression profiling and molecular analysis. The role of ELK3 in determining the immunosensitivity of TNBC to NK cells was investigated in terms of mitochondrial fission-fusion transition and reactive oxygen species concentration both in vitro and in vivo.
resultsELK3-dependent mitochondrial fission-fusion status was linked to the mitochondrial superoxide concentration in TNBCs and was a main determinant of NK cell-mediated immune responses. We identified mitochondrial dynamics proteins of 51 (Mid51), a major mediator of mitochondrial fission, as a direct downstream target of ELK3 in TNBCs. Also, we demonstrated that expression of ELK3 correlated inversely with that of Mid51, and that the ELK3-Mid51 axis is associated directly with the status of mitochondrial dynamics. METABRIC analysis revealed that the ELK3-Mid51 axis has a direct effect on the immune score and survival of patients with TNBC.
conclusionsTaken together, the data suggest that NK cell responses to TNBC are linked directly to ELK3 expression levels, shedding new light on strategies to improve the efficacy of NK cell-based immunotherapy of TNBC.
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