ARMC10

Last update 08 May 2025

Basic Info

Synonyms

armadillo repeat containing 10, Armadillo repeat-containing protein 10, ARMC10

+ [3]

Introduction

May play a role in cell survival and cell growth. May suppress the transcriptional activity of p53/TP53.

100 Clinical Results associated with ARMC10

100 Translational Medicine associated with ARMC10

0 Patents (Medical) associated with ARMC10

Literatures (Medical) associated with ARMC10

01 May 2025·Molecular Carcinogenesis

ARMC10 Drives Glioblastoma Progression Through Activating Notch Pathway

Article

Author: Feng, Bin ; Chen, Lin ; Xing, Yi ; Gao, Taihong

ABSTRACTThis study aimed to check the biological functions and uncover the mechanism of armadillo repeat protein C10 (ARMC10) in glioblastoma (GBM). The expression and potential mechanisms of ARMC10 in GBM were analyzed by bioinformatics analysis. In GBM cells, function‐loss experiments were used to evaluate the influences of ARMC10 on cell proliferation, cell invasion, lipid levels, and cell migration by colony formation assay, 5‐ethynyl‐2′‐deoxyuridine staining, cell counting kit‐8 assay, transwell assay, BODIPY staining, and wound healing assay. Mouse xenograft models were constructed to validate the influences of ARMC10 in vivo. ARMC10 levels in GBM were upregulated, and patients with low ARMC10 levels displayed a better prognosis. ARMC10 knockdown resulted in a decrease of GBM cell invasion, migration, and proliferation. GSEA showed that ARMC10 was positively associated with the Notch pathway and fatty acid metabolism. ARMC10 knockdown reduced the levels of triglyceride, cholesterol, and lipid, and inhibited the expression of proteins related to fatty acid metabolism and Notch pathway. Moreover, notch receptor 1 (Notch1) overexpression reversed the inhibition of cell proliferation, fatty acid metabolism, and invasion induced by ARMC10 knockdown. In vivo, ARMC10 knockdown suppressed tumor growth. RMC10 knockdown suppressed GBM malignant progression, which had a bearing on Notch pathway.

01 Jun 2024·Journal of Cellular and Molecular Medicine

ARMC10 regulates mitochondrial dynamics and affects mitochondrial function via the Wnt/β‐catenin signalling pathway involved in ischaemic stroke

Article

Author: Zhou, Baixue ; Bie, Xiaoshuai ; Li, Zhihao ; Luan, Yingying ; Jia, Jing ; Huang, Yanyang ; Peng, Yue ; Yang, Dongzhi ; Zhang, Zhaojing ; Zhang, Chi ; Zheng, Hong ; Xu, Yatian ; Xu, Ruochen ; He, Ying ; Han, Tianyi

AbstractMitochondrial dynamics has emerged as an important target for neuronal protection after cerebral ischaemia/reperfusion. Therefore, the aim of this study was to investigate the mechanism by which ARMC10 regulation of mitochondrial dynamics affects mitochondrial function involved in ischaemic stroke (IS). Mitochondrial morphology was detected by laser scanning confocal microscopy (LSCM), and mitochondrial ultrastructural alterations were detected by electron microscopy. The expression of mitochondrial dynamics‐related genes Drp1, Mfn1, Mfn2, Fis1, OPA1 and ARMC10 and downstream target genes c‐Myc, CyclinD1 and AXIN2 was detected by RT‐qPCR. Western blot was used to detect the protein expression of β‐catenin, GSK‐3β, p‐GSK‐3β, Bcl‐2 and Bax. DCFH‐DA fluorescent probe was to detect the effect of ARMC10 on mitochondrial ROS level, Annexin V‐FITC fluorescent probe was to detect the effect of ARMC10 on apoptosis, and ATP assay kit was to detect the effect of ARMC10 on ATP production. Mitochondrial dynamics was dysregulated in clinical IS samples and in the OGD/R cell model, and the relative expression of ARMC10 gene was significantly decreased in IS group (p < 0.05). Knockdown and overexpression of ARMC10 could affect mitochondrial dynamics, mitochondrial function and neuronal apoptosis. Agonist and inhibitor affected mitochondrial function and neuronal apoptosis by targeting Wnt/β‐Catenin signal pathway. In the OGD/R model, ARMC10 affected mitochondrial function and neuronal apoptosis through the mechanism that regulates Wnt/β‐catenin signalling pathway. ARMC10 regulates mitochondrial dynamics and protects mitochondrial function by activating Wnt/β‐catenin signalling pathway, to exert neuroprotective effects.

19 Oct 2023·International journal of molecular sciences

Inflammatory Mediators of Axon Regeneration in the Central and Peripheral Nervous Systems.

Review

Author: Xie, Lili ; Benowitz, Larry I ; Yin, Yuqin

Although most pathways in the mature central nervous system cannot regenerate when injured, research beginning in the late 20th century has led to discoveries that may help reverse this situation. Here, we highlight research in recent years from our laboratory identifying oncomodulin (Ocm), stromal cell-derived factor (SDF)-1, and chemokine CCL5 as growth factors expressed by cells of the innate immune system that promote axon regeneration in the injured optic nerve and elsewhere in the central and peripheral nervous systems. We also review the role of ArmC10, a newly discovered Ocm receptor, in mediating many of these effects, and the synergy between inflammation-derived growth factors and complementary strategies to promote regeneration, including deleting genes encoding cell-intrinsic suppressors of axon growth, manipulating transcription factors that suppress or promote the expression of growth-related genes, and manipulating cell-extrinsic suppressors of axon growth. In some cases, combinatorial strategies have led to unprecedented levels of nerve regeneration. The identification of some similar mechanisms in human neurons offers hope that key discoveries made in animal models may eventually lead to treatments to improve outcomes after neurological damage in patients.

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ARMC10

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