Ask about this productRelated genes to: Armcx1 Blocking Peptide
- Gene:
- ARMCX1 NIH gene
- Name:
- armadillo repeat containing X-linked 1
- Previous symbol:
- -
- Synonyms:
- ALEX1, GASP7
- Chromosome:
- Xq22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-10
- Date modifiied:
- 2018-04-26
Related products to: Armcx1 Blocking Peptide
Related articles to: Armcx1 Blocking Peptide
- Tumor heterogeneity challenges the accuracy of existing prognostic models for cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC). Prognostic models that correct for tumor heterogeneity remain unexplored. - Source: PubMed
Publication date: 2026/03/31
Tang XiaoboZheng QingLi XinWang Kaisong - BACKGROUND: Armadillo repeat-containing X-linked 1 (ARMCX1) has been reported to exhibit a suppressive effect in a variety of solid tumors. However, neither its biological role nor its potential mechanism of action has yet been reported in nasopharyngeal carcinoma (NPC). METHODS: Immunohistochemical staining of an NPC tissue microarray was performed to evaluate the clinicopathologic association between ARMCX1 and NPC patients. The effect of ARMCX1 on the growth, migratory, and invasive capacities of NPC cells was assessed in vitro using colony formation, Cell Counting Kit-8 (CCK-8), 5-ethynyl-2’-deoxyuridine (EdU), scratch, and Transwell assays. A subcutaneous graft tumor model was implemented to investigate the impact of ARMCX1 on the tumor growth of NPC cells in vivo. Western blotting, immunofluorescence staining, and cycloheximide and proteasome inhibitor experiments were employed to investigate the potential molecular mechanisms of ARMCX1 in NPC RESULTS: Overexpression of ARMCX1 effectively inhibited the growth, migration, and invasion in NPC cells. Western blotting, co-immunoprecipitation, immunofluorescence, and cycloheximide and proteasome inhibitor experiments revealed that ARMCX1 mediated the β-catenin ubiquitination and degradation via recruiting tripartite motif-containing protein 21 (TRIM21), thereby suppressing cell cycle progression and epithelial–mesenchymal transition. Final rescue assays demonstrated that β-catenin reversed ARMCX1-mediated suppression of NPC cell proliferation, migration, and invasion. CONCLUSIONS: ARMCX1 attenuates NPC cell proliferation, migration, and invasion by binding β-catenin and promoting its ubiquitination-dependent degradation via TRIM21. Hence, ARMCX1 may serve as a potential molecular target for therapeutic intervention in NPC. - Source: PubMed
Publication date: 2026/01/14
Hu ZheZhuo EnqingGuo JiankangWu YilinSun XiaoouQiu HoukuangZhou YangfanTan XiZhang Xuhui - A complex and gradual process, the epithelial-mesenchymal transition (EMT) occurs both during embryonic development and tumor progression. Cells undergo a transition from an epithelial to a mesenchymal state throughout this process. More and more evidence points to EMT as a cause of increased metastatic spread of prostate cancer (PCa), along with stemness enhancement and therapy resistance. Here, we used bioinformatic methods to analyze gene expression microarray data, single-cell RNA sequencing, oncogenes, and tumor suppressor genes (TSGs) in order to reconstruct the network of differentially expressed genes (DEGs) involved in the epithelial-mesenchymal transition with PCa. No prior study has documented this sort of analysis. We next validated our results using data from the Cancer Genome Atlas (TCGA), which included microarray and single-cell RNA sequencing. Potentially useful in PCa diagnosis and treatment are extracellular matrix in epithelial-mesenchymal transition genes, including , , , , , , and . In this study, we aimed to shed light on the molecular characteristics and pathways of DEGs in PCa, as well as to identify possible biomarkers that are important in the development and advancement of this cancer. These insights have important implications for understanding prostate cancer progression and for the development of therapeutic strategies targeting ECM-mediated pathways. - Source: PubMed
Publication date: 2025/09/03
Shakeri Abroudi AliMashhouri Moghaddam MahtabHashemi Karoii DanialDjamali MelikaAzizi HosseinSkutella Thomas - Armadillo Repeat Containing X-Linked 1 (ARMCX1), a member of the ARM Repeat X-linked protein family, exerts inhibitory function in various tumors. However, its biological role in lung adenocarcinoma (LUAD) and the underlying molecular mechanisms require further exploration. - Source: PubMed
Publication date: 2024/09/16
Hu ZheWu YilinSun XiaoouTong YanliQiu HoukuangZhuo Enqing - Armadillo repeat-containing X-linked protein-1 (Armcx1) is a poorly characterized transmembrane protein that regulates mitochondrial transport in neurons. Its overexpression has been shown to induce neurite outgrowth in embryonic neurons and to promote retinal ganglion cell (RGC) survival and axonal regrowth in a mouse optic nerve crush model. In order to evaluate the functions of endogenous Armcx1 in vivo, we have created a conditional Armcx1 knockout mouse line in which the entire coding region of the Armcx1 gene is flanked by loxP sites. This Armcx1 line was crossed with mouse strains in which Cre recombinase expression is driven by the promoters for β-actin and Six3, in order to achieve deletion of Armcx1 globally and in retinal neurons, respectively. Having confirmed deletion of the gene, we proceeded to characterize the abundance and morphology of RGCs in Armcx1 knockout mice aged to 15 months. Under normal physiological conditions, no evidence of aberrant retinal or optic nerve development or RGC degeneration was observed in these mice. The Armcx1 mouse should be valuable for future studies investigating mitochondrial morphology and transport in the absence of Armcx1 and in determining the susceptibility of Armcx1-deficient neurons to degeneration in the setting of additional heritable or environmental stressors. - Source: PubMed
Bright Cora LBomze Howard MBhaumik MantuKay Jeremy NCartoni RomainGospe Sidney M