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Nmi has a distinct role in the differentiation process of mammary luminal epithelial cell compartment and developmental aberrations resulting from Nmi absence contribute to metastasis.
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These results revealed that IRF-1 is involved in the IFN-inducible expression of Nmi.
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Our study showed that NMI suppressed tumor growth by inhibiting PI3K/AKT, MMP2/MMP9, COX-2/PGE2 signaling pathways and p300-mediated NF-kappaB acetylation, and predicted a favorable prognosis in human lung adenocarcinomas, suggesting that NMI was a potential tumor suppressor in lung cancer.
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results provide new insights into understanding the regulatory mechanism of cancer stem cells and suggest that the NMI-YY1-hTERT signaling axis may be a potential therapeutic target for breast cancers.
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Damage-associated molecular patterns (DAMP) are important mediators of innate immunity. Here the authors show that N-myc and STAT interactor (NMI) and interferon-induced protein 35 (IFP35) act as DAMPs to promote inflammation by activating macrophages via the Toll-like receptor 4 and NF-kappaB pathways.
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These investigations demonstrated etoposide-induced NMI can suppress tumor proliferation and promote cell apoptosis by activating the ARF-p53 signaling pathway in lung carcinoma. Our results provide an alternative mechanism for etoposide in lung carcinoma and suggest NMI has a critical role in suppressing lung carcinoma progression.
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Data suggest that N-myc (and STAT) interactor (NMI) could improve its downstream target bradykinin B2 receptor (BDKRB2) expression to induce extracellular signal-regulated kinases (ERK) 1/2 activation, and thereby further evoke malignant progression of hepatocellular carcinoma (HCC).
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N-Myc-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-kappaB/p65 in histone deacetylase-dependent manner.
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N-myc and STAT interactor sensitizes breast cancer cells to cisplatin treatment through DRAM1 dependent autophagy.
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Results show that aberrant miR-29 expression may account for reduced NMI expression in breast tumors and mesenchymal phenotype of cancer cells that promotes invasive growth.
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The results showed that SARS coronavirus protein 6 can promote the ubiquitin-dependent proteosomal degradation of Nmi.
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overexpression or depletion of NMI revealed its regulation on G1/S progression and cell proliferation (both in vitro and in vivo), and this effect was partially dependent on STAT1, which interacted with and was regulated by NMI.
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Trim21 regulates Nmi-IFI35 complex-mediated inhibition of innate antiviral response
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Its potential function in transcriptional activation of NMI.
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identified NMI induction as a novel negative feedback mechanism that decreases IRE1alpha-dependent activation of JNK and apoptosis in cytokine-exposed beta cells
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Thus our work reveals a novel NMI-mediated, transcription-independent ARF induction pathway in response to cellular stresses.
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Dissociation of the IFN-induced protein NMI from IFP35 is a newly defined specific cytoplasmic event occurring during apoptosis.
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complex with BRCA1 and c-Myc inhibits c-Myc-induced human telomerase reverse transcriptase gene promoter activity in breast cancer
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Apoptin mutant T1 still interacted with Nmi, suggesting that its C-terminal 11 AA was not essential for the interaction.
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STAT1 and Nmi are downstream targets of Ets-1 in MCF-7 human breast cancer cells
