Abstract
Introduction: Mitochondrial fission regulator 2 (MTFR2) belongs to the MTFR family, and 2 isoforms of MTFR2 are produced by alternative splicing. The role of MTFR2 in breast cancer (BC) remains unknown.Results: MTFR2 was upregulated in BC tissues and was strongly associated with tumor characteristics. Moreover, Kaplan-Meier and Cox proportional hazards analyses indicated that high MTFR2 expression was related to poor overall survival. In addition, the capacity for migration and invasion decreased in two BC cell lines after knockdown of MTFR2. The epithelial-mesenchymal transition pathway was inhibited in MTFR2-silenced cells. MTFR2 can switch glucose metabolism from OXPHS to glycolysis in a HIF1α- and HIF2α-dependent manner.Conclusion: Taken together, our results indicate that increased expression of MTFR2 is associated with tumour progression in breast cancer cells through switching glucose metabolism from OXPHS to glycolysis in a HIF1α- and HIF2α-dependent manner.Materials and methods: We obtained data from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) to analyse MTFR2 expression in BC. The prognostic value of MTFR2 expression was assessed using the Kaplan-Meier method. The biological influence of MTFR2 on BC cell lines was studied using proliferation, Transwell migration, invasion and mitochondrial function assays.
Highlights
Mitochondrial fission regulator 2 (MTFR2) belongs to the MTFR family, and 2 isoforms of MTFR2 are produced by alternative splicing
We compared 1085 breast cancer (BC) tissues and 112 normal tissues from The Cancer Genome Atlas (TCGA), and the results showed that MTFR2 expression was significantly higher in tumour tissues than in normal tissues (p
We analysed MTFR2 expression from the GSE38959 (p
Summary
Mitochondrial fission regulator 2 (MTFR2) belongs to the MTFR family, and 2 isoforms of MTFR2 are produced by alternative splicing. Conclusion: Taken together, our results indicate that increased expression of MTFR2 is associated with tumour progression in breast cancer cells through switching glucose metabolism from OXPHS to glycolysis in a HIF1α- and HIF2α-dependent manner. The biological influence of MTFR2 on BC cell lines was studied using proliferation, Transwell migration, invasion and mitochondrial function assays. The shape of the mitochondrial network results from the cumulative activity of two opposing processes: fusion and fission [7] These processes collaborate to ensure the homeostatic maintenance of mitochondrial function, the bioenergetics of the cell, and the commitment to mitosis [8]. Recent studies have revealed that abnormal mitochondrial fission is involved in the pathogenesis of many diseases and that it contributes to the progression of tumours [10, 11]. The expression and biological functions of MTFR2 in BC remain unclear
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