ArticleOncogene2014
Identification of epithelial stromal interaction 1 as a novel effector downstream of Krüppel-like factor 8 in breast cancer invasion and metastasis.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- EPSTI1 as an immune biomarker predicts the prognosis of patients with stage III colon cancer.Frontiers in immunology · 2022Pooled it
- Krüppel-like factor 10 promotes the progression of breast cancer by activating canonical NF-κB signaling.iScience · 2026Article
- Implications of Krüppel-like factor signaling in neuroinflammation for neurodegenerative diseases.American journal of translational research · 2025Review
- Elevated expression of hsa_circ_0000479 in neutrophils correlates with features of systemic lupus erythematosus.Annals of medicine · 2024Article
- Exosomal circ-0100519 promotes breast cancer progression via inducing M2 macrophage polarisation by USP7/NRF2 axis.Clinical and translational medicine · 2024Article
- Identification of EPSTI1 as a new potential biomarker for SLE based on GEO database.Clinical rheumatology · 2024Article
- High-resolution transcriptomics analysis of CXCL13Journal of thoracic disease · 2024Article
- Epsti1 Regulates the Inflammatory Stage of Early Muscle Regeneration through STAT1-VCP Interaction.International journal of biological sciences · 2024Article
- Sevoflurane suppresses the malignant progression of breast cancer via the hsa_circ_0000129/miR-578/EPSTI1 axis.Thoracic cancer · 2023Article
- Krüppel-like factors in tumors: Key regulators and therapeutic avenues.Frontiers in oncology · 2023Review
- Tbc1d10c is a selective, constitutive suppressor of the CD8 T-cell anti-tumor response.Oncoimmunology · 2022Article
- KLF8 promotes invasive outgrowth of breast cancer by inducing filopodium-like protrusions via CXCR4.American journal of translational research · 2022Article
- Contrasting functions of the epithelial‑stromal interaction 1 gene, in human oral and lung squamous cell cancers.Oncology reports · 2022Article
- KSR1- and ERK-dependent translational regulation of the epithelial-to-mesenchymal transition.eLife · 2021Article
- Sensitization of breast cancer to Herceptin by redox active nanoparticles.American journal of cancer research · 2021Article
- Role of krüppel-like factor 8 for therapeutic drug-resistant multi-organ metastasis of breast cancer.American journal of cancer research · 2021Article
- Epigenetic programming underpins B cell dysfunction in human SLE.Nature immunology · 2019Article
- circEPSTI1 regulates ovarian cancer progression via decoying miR-942.Journal of cellular and molecular medicine · 2019Article
- Regulation of Krüppel-like factor 8 by the NEDD4 E3 ubiquitin ligase.American journal of translational research · 2019Article
- Molecular classification and subtype-specific characterization of skin cutaneous melanoma by aggregating multiple genomic platform data.Journal of cancer research and clinical oncology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Krüppel-like factor 8 (KLF8) is a transcriptional factor critical for metastatic progression of breast cancer. Epithelial stromal interaction 1 (EPSTI1), a recently identified stromal fibroblast-induced gene in non-invasive breast cancer cells is highly overexpressed in invasive breast carcinomas. The function and regulation of EPSTI1, however, remain largely unknown. In this paper, we report a novel KLF8 to EPSTI1 signaling pathway in breast cancer. Using various expression analyses, we revealed a high co-overexpression of KLF8 and EPSTI1 in invasive human breast cancer cells and patient tumors. Ectopic overexpression of KLF8 in the non-invasive MCF-10A cells induced the EPSTI1 expression, whereas KLF8 knockdown from the invasive, MDA-MB-231 cells decreased the EPSTI1 expression. Promoter activation and binding analyses indicated that KLF8 promoted the EPSTI1 expression by directly acting on the EPSTI1 gene promoter. EPSTI1 knockdown dramatically reduced the KLF8-promoted MCF-10A cell invasion, and ectopic expression of EPSTI1 in the non-invasive MCF-7 cells is sufficient to induce the cell invasion. Experiments using nude mice demonstrated that the ectopic EPSTI1 granted the MCF-7 cells capability of both invasive growth in the breasts and metastasis to the lungs. Using co-immunoprecipitation coupled with mass spectrometry, we discovered that EPSTI1 interacts with the valosin-containing protein (VCP), resulting in the degradation of IκBα and subsequent activation of NF-κB in the nucleus. These findings suggest a novel KLF8 to EPSTI1 to VCP to NF-κB signaling mechanism potentially critical for breast cancer invasion and metastasis.
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Registered trials
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