MIEF2

Last update 08 May 2025

Basic Info

Synonyms

MGC23130, MiD49, MIEF2

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Introduction

Mitochondrial outer membrane protein involved in the regulation of mitochondrial organization (PubMed:29361167). It is required for mitochondrial fission and promotes the recruitment and association of the fission mediator dynamin-related protein 1 (DNM1L) to the mitochondrial surface independently of the mitochondrial fission FIS1 and MFF proteins. Regulates DNM1L GTPase activity.

100 Clinical Results associated with MIEF2

100 Translational Medicine associated with MIEF2

0 Patents (Medical) associated with MIEF2

Literatures (Medical) associated with MIEF2

01 May 2025·Journal of Cell Science

Mitochondrial fission – changing perspectives for future progress

Review

Author: Liu, Ao ; Kamerkar, Sukrut C. ; Higgs, Henry N.

ABSTRACTMitochondrial fission is important for many aspects of cellular homeostasis, including mitochondrial distribution, stress response, mitophagy, mitochondrially derived vesicle production and metabolic regulation. Several decades of research has revealed much about fission, including identification of a key division protein – the dynamin Drp1 (also known as DNM1L) – receptors for Drp1 on the outer mitochondrial membrane (OMM), including Mff, MiD49 and MiD51 (also known as MIEF2 and MIEF1, respectively) and Fis1, and important Drp1 regulators, including post-translational modifications, actin filaments and the phospholipid cardiolipin. In addition, it is now appreciated that other organelles, including the endoplasmic reticulum, lysosomes and Golgi-derived vesicles, can participate in mitochondrial fission. However, a more holistic understanding of the process is lacking. In this Review, we address three questions that highlight knowledge gaps. First, how do we quantify mitochondrial fission? Second, how does the inner mitochondrial membrane (IMM) divide? Third, how many ‘types’ of fission exist? We also introduce a model that integrates multiple regulatory factors in mammalian mitochondrial fission. In this model, three possible pathways (cellular stimulation, metabolic switching or mitochondrial dysfunction) independently initiate Drp1 recruitment at the fission site, followed by a shared second step in which Mff mediates subsequent assembly of a contractile Drp1 ring. We conclude by discussing some perplexing issues in fission regulation, including the effects of Drp1 phosphorylation and the multiple Drp1 isoforms.

01 Jan 2025·Translational Cancer Research

Oxidative phosphorylation-related genes for prognosis and tumor microenvironment in breast cancer

Article

Author: Dong, Shu-Feng ; Wang, Chun-Lei ; Xia, Man-Zhi

BackgroundOxidative phosphorylation (OXPHOS) is a major energy resource occurring in mitochondria. Targeting OXPHOS-related genes has emerged as potential targets for cancer therapy. This study aimed to explore the significance of OXPHOS-related genes in breast cancer (BRCA).MethodsDifferentially expressed genes (DEGs) related to OXPHOS in BRCA were identified using packages of Limma and VennDiagram using the data from public databases. A prognostic model based on differentially expressed OXPHOS-related genes was constructed using least absolute shrinkage and selection operator Cox regression analyses and then evaluated through Kaplan-Meier and receiver operator characteristic (ROC) curves. Additionally, gene set variate analysis (GSVA) and gene set enrichment analysis (GSEA) were performed to explore the potential pathways involved in BRCA. Furthermore, the tumor microenvironment (TME) difference between low- and high-risk BRCA groups was investigated. The prognostic significance of hub genes was then examined. We conducted a protein-protein interaction (PPI) network to uncover the potential gene interactions and identify key genes, whose expressions were validated in cells.ResultsOur analyses revealed 234 differentially expressed OXPHOS-related genes, from which a nine-gene (ATP5PF, FOXP3, IGF2, IREB2, MIEF2, NOTCH1, PDE12, SHC1, and UCP3) prognostic model was constructed. Patients in the high-risk group exhibited poorer survival outcomes and a suppressed immune microenvironment compared to the low-risk group. Additionally, except for IGF2, abnormal expression levels of hub genes were significantly associated with poor prognosis of BRCA patients. GSVA and GSEA highlighted the involvement of TME-related pathways, such as transforming growth factor beta (TGF-β) and mechanistic target of rapamycin (mTOR) signaling pathways. PPI network identified 4 common genes that interacted with all hub genes. The in vitro experiment on the key genes showed a consistent result with the bioinformatics finding.ConclusionsOur study provides insights into the prognostic biomarkers and molecular mechanisms in BRCA, offering potential therapeutic avenues and guiding personalized treatment strategies for improved patient outcomes.

01 Nov 2024·Acta Biochimica et Biophysica Sinica

PRR34-AS1 promotes mitochondrial division and glycolytic reprogramming in hepatocellular carcinoma cells through upregulation of MIEF2

Article

Author: Wang, Lin ; Feng, Huijing ; Song, Dong ; Yang, Xuejing ; Ti, Gang ; Wang, Kun ; Kim, Jonghwa

LncRNA PRR34-AS1 overexpression promotes the proliferation and invasion of hepatocellular carcinoma (HCC) cells, but whether it affects HCC energy metabolism remains unclear. Mitochondrial division and glycolytic reprogramming play important roles in tumor development. In this study, the differential expression of PRR34-AS1 is explored via TCGA analysis, and higher levels of PRR34-AS1 are detected in patients with liver cancer than in healthy individuals. A series of experiments, such as CCK-8, PCR, and immunofluorescence staining, reveal that the proliferation, invasion, glycolysis, and mitochondrial division of PRR34-AS1-overexpressing hepatoma cells are significantly promoted. TCGA analysis and immunohistochemistry reveal high expression of the mitochondrial dynamin MIEF2 in liver cancer tissues. Dual-luciferase reporter assays confirm that miR-498 targets and binds to mitochondrial elongation factor 2 (MIEF2). In addition, we show that PRR34-AS1 can sponge miR-498. Therefore, we further investigate the effects of the lncRNA PRR34-AS1/miR-498/MIEF2 axis on the growth, glucose metabolism, and mitochondrial division in hepatocellular carcinoma cells. A series of experiments are performed on hepatocellular carcinoma cells after different treatments. The results show that the proliferative activity, invasive ability, and glycolytic level of hepatocellular carcinoma cells are decreased in HCC cells with low PRR34-AS1 expression, and the miR-498 expression level is increased in these cells. Inhibition of miR-498 or overexpression of MIEF2 restored the proliferative activity, invasive ability, glycolysis, and mitochondrial division in hepatocellular carcinoma cells. Thus, PRR34-AS1 regulates MIEF2 by sponging miR-498, thereby promoting mitochondrial division, mediating glycolytic reprogramming and ultimately driving the growth and invasion of HCC cells. Furthermore, in vivo mouse experiments yield results similar to those of the in vitro experiments, verifying the above results.

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MIEF2

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