ArticleMolecular cancer2017
Downregulation of NMI promotes tumor growth and predicts poor prognosis in human lung adenocarcinomas.
Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
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- Antitumor Activity of USP7 Inhibitor GNE-6776 in Non-Small Cell Lung Cancer Involves Regulation of Epithelial-Mesenchymal Transition, Cell Cycle, Wnt/β-Catenin, and PI3K/AKT/mTOR Pathways.Pharmaceuticals (Basel, Switzerland) · 2025Article
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- USP44 regulates HEXIM1 stability to inhibit tumorigenesis and metastasis of oral squamous cell carcinoma.Biology direct · 2024Article
- Multi‑omics identification of a signature based on malignant cell-associated ligand-receptor genes for lung adenocarcinoma.BMC cancer · 2024Article
- N-Myc and STAT Interactor is an Endometriosis Suppressor.International journal of molecular sciences · 2024Article
- Targeting EMT using low-dose Teniposide by downregulating ZEB2-driven activation of RNA polymerase I in breast cancer.Cell death & disease · 2024Article
- Implications of different cell death patterns for prognosis and immunity in lung adenocarcinoma.NPJ precision oncology · 2023Article
- Development of a Macrophage-Related Risk Model for Metastatic Melanoma.International journal of molecular sciences · 2023Article
- FOXA1-induced LINC00621 promotes lung adenocarcinoma progression via activating the TGF-β signaling pathway.Thoracic cancer · 2023Article
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- Clinical predictors of treatment efficacy and a prognostic nomogram in patients with lung adenocarcinoma receiving immune checkpoint inhibitors: a retrospective study.Journal of thoracic disease · 2022Article
- Curcumenol triggered ferroptosis in lung cancer cells via lncRNA H19/miR-19b-3p/FTH1 axis.Bioactive materials · 2022Article
- HNRNPK/CLCN3 axis facilitates the progression of LUAD through CAF-tumor interaction.International journal of biological sciences · 2022Article
- GNAI2 Is a Risk Factor for Gastric Cancer: Study of Tumor Microenvironment (TME) and Establishment of Immune Risk Score (IRS).Oxidative medicine and cellular longevity · 2022Article
- MiR-96-5p Facilitates Lung Adenocarcinoma Cell Phenotypes by Inhibiting FHL1.Computational and mathematical methods in medicine · 2022Article
- NMI: a potential biomarker for tumor prognosis and immunotherapy.Frontiers in pharmacology · 2022Article
- Disruption of STAT5A and NMI signaling axis leads to ISG20-driven metastatic mammary tumors.Oncogenesis · 2021Article
- Single-Molecule RNA Sequencing Reveals IFNγ-Induced Differential Expression of Immune Escape Genes in Merkel Cell Polyomavirus-Positive MCC Cell Lines.Frontiers in microbiology · 2021Article
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Authors and funding
20 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundN-myc (and STAT) interactor (NMI) plays vital roles in tumor growth, progression, and metastasis. In this study, we identified NMI as a potential tumor suppressor in lung cancer and explored its molecular mechanism involved in lung cancer progression.
methodsHuman lung cancer cell lines and a mouse xenograft model was used to study the effect of NMI on tumor growth. The expression of NMI, COX-2 and relevant signaling proteins were examined by Western blot. Tissue microarray immunohistochemical analysis was performed to assess the correlation between NMI and COX-2 expression in lung cancer patients.
resultsNMI was highly expressed in normal lung cells and tissues, but lowly expressed in lung cancer cells and tissues. Overexpression of NMI induced apoptosis, suppressed lung cancer cell growth and migration, which were mediated by up-regulation of the cleaved caspase-3/9 and down-regulation of phosphorylated PI3K/AKT, MMP2/MMP9, β-cadherin, and COX-2/PGE2. In contrast, knockdown of NMI promoted lung cancer cell colony formation and migration, which were correlated with the increased expression of phosphorylated PI3K/AKT, MMP2/MMP9, β-cadherin and COX-2/PGE2. Further study showed that NMI suppressed COX-2 expression through inhibition of the p50/p65 NF-κB acetylation mediated by p300. The xenograft lung cancer mouse models also confirmed the NMI-mediated suppression of tumor growth by inhibiting COX-2 signaling. Moreover, tissue microarray immunohistochemical analysis of lung adenocarcinomas also demonstrated a negative correlation between NMI and COX-2 expression. Kaplan-Meier analysis indicated that the patients with high level of NMI had a significantly better prognosis.
conclusionsOur study showed that NMI suppressed tumor growth by inhibiting PI3K/AKT, MMP2/MMP9, COX-2/PGE2 signaling pathways and p300-mediated NF-κB 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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