ArticleJournal of hematology & oncology2018
NOD-like receptor X1 functions as a tumor suppressor by inhibiting epithelial-mesenchymal transition and inducing aging in hepatocellular carcinoma cells.
Article in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- NLRX1 Drives Prostate Cancer Progression Through Activation of AKT and ERK Signaling Pathways.International journal of biological sciences · 2026Article
- Harnessing NLRX1: a new frontier in mitigating inflammation in pulmonary hypertension.Respiratory research · 2025Article
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- Insights into the structure of NLR family member X1: Paving the way for innovative drug discovery.Computational and structural biotechnology journal · 2024Article
- Activation of NOD1 on tumor-associated macrophages augments CD8Science advances · 2024Article
- Bioinformatics analysis and experimental verification of NLRX1 as a prognostic factor for esophageal squamous cell carcinoma.Oncology letters · 2024Article
- Targeting cell death pathways in intestinal ischemia-reperfusion injury: a comprehensive review.Cell death discovery · 2024Review
- Signature construction and molecular subtype identification based on liver-specific genes for prediction of prognosis, immune activity, and anti-cancer drug sensitivity in hepatocellular carcinoma.Cancer cell international · 2024Article
- Cellular Context Dictates the Suppression or Augmentation of Triple-Negative Mammary Tumor Metastasis by NLRX1.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- NLRX1 functions as a tumor suppressor in Pan02 pancreatic cancer cells.Frontiers in oncology · 2023Article
- The role of non-coding RNAs in myocarditis: a narrative review.Annals of translational medicine · 2022Review
- PLOD3 contributes to HER-2 therapy resistance in gastric cancer through FoxO3/Survivin pathway.Cell death discovery · 2022Article
- Sex-Biased Control of Inflammation and Metabolism by a Mitochondrial Nod-Like Receptor.Frontiers in immunology · 2022Article
- Ubiquitin-related molecular classification and risk stratification of hepatocellular carcinoma.Molecular therapy oncolytics · 2021Article
- A prognostic model based on seven immune-related genes predicts the overall survival of patients with hepatocellular carcinoma.BioData mining · 2021Article
- NOD-like receptor X1, tumor necrosis factor receptor-associated factor 6 and NF-κB are associated with clinicopathological characteristics in gastric cancer.Experimental and therapeutic medicine · 2021Article
- NLR in eXile: Emerging roles of NLRX1 in immunity and human disease.Immunology · 2021Review
- Risk Score Based on Two microRNAs as a Prognostic Marker of Hepatocellular Carcinoma and the Corresponding Competitive Endogenous RNA Network.International journal of general medicine · 2021Article
- Review
- Bioinformatics analysis of different candidate genes involved in hepatocellular carcinoma induced by HepG2 cells or tumor cells of patients.The Journal of international medical research · 2020Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study was performed to investigate the role of nucleotide-binding oligomerization domain (NOD)-like receptor X1 (NLRX1) in regulating hepatocellular carcinoma (HCC) progression.
methodsExpression levels of NLRX1 in clinical specimens and cell lines were determined by reverse transcription-polymerase chain reaction (RT-PCR) and western blot (WB). Transwell assays were conducted to evaluate the effect of NLRX1 on cell invasion, and flow cytometry was used to assess apoptosis. Expression patterns of key molecules in the phosphoinositide 3-kinase (PI3K)-AKT pathways were determined via WB. The effect of NLRX1 on cell senescence was evaluated with β-galactosidase assays. Kaplan-Meier analyses and Cox regression models were used for prognostic evaluation.
resultsNLRX1 was downregulated in tumor tissue compared with adjacent normal liver tissue. Low tumor NLRX1 expression was identified as an independent indicator for HCC prognosis (recurrence: hazard ratio [HR] 1.87, 95% confidence interval [CI] 1.26-2.76, overall survival [OS] 2.26, 95% CI 1.44-3.56). NLRX1 over-expression (OE) significantly inhibited invasiveness ability and induced apoptosis in HCC cells. In vivo experiments showed that NLRX1 knock-down (KD) significantly promoted HCC growth. Mechanistically, NLRX1 exhibited a suppressor function by decreasing phosphorylation of AKT and thus downregulating Snail1 expression, which inhibited epithelial-mesenchymal-transition (EMT) in HCC cells. Moreover, NLRX1 OE could induce cell senescence via an AKT-P21-dependent manner.
conclusionsNLRX1 acted as a tumor suppressor in HCC by inducing apoptosis, promoting senescence, and decreasing invasiveness by repressing PI3K-AKT signaling pathway. Future investigations will focus on restoring expression of NLRX1 to provide new insights into HCC treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.