MTFR2 Promotes the Proliferation, Migration, and Invasion of Oral Squamous Carcinoma by Switching OXPHOS to Glycolysis

Abstract

MTFR2 is an oncogene involved in the progression of cancer, its' potential mechanism in oral squamous carcinoma remains unknown. The aim of this study was to uncover the bio-function and the mechanism of MTFR2 in the progression of oral squamous carcinoma. We scanned TCGA database to identify MTFR2 as dysregulated genes. qRT-PCR and Western blotting assays were applied to detect the expression pattern of MTFR2 in oral squamous carcinoma. We next established stable MTFR2-overexpressing and MTFR2 knocking down cell lines. A series of experiments were applied and the results indicated that MTFR2 was upregulated in cancer tissue and negatively correlated with the overall survival (OS) of patients in both the TCGA database and our inhouse database. Following experiments showed that MTFR2 promotes proliferation, migration and invasion in an oral squamous carcinoma cell line by switching OXPHOS to glycolysis.

Upregulated Expression of MTFR2 as a Novel Biomarker Predicts Poor Prognosis in Hepatocellular Carcinoma by Bioinformatics Analysis

“…APE1 methylation deletion reduces mitochondrial translocation and increases mitochondrial DNA damage and cytochrome c release after stimulation, indicating that APE1 methylation promotes mitochondrial translocation and protects cells from oxidative damage. Previous studies have found that MTFR2 plays an oncogene role in BC and oral squamous cell carcinoma [11,12]. The authors' results using the Simple Modular Architecture Research Tool data resource illustrated that the level of MTFR2 methylation is significantly abnormal in HCC tissues.…”

“…Wang et al found that MTFR2 converts oxidative phosphorylation into glycolysis, thus promoting the growth, migration and infiltration of cancer cells [12]. The mechanism linked to the growth of HCC has not been reported in the literature.…”

“…Downregulation of FGD1 expression can significantly decrease the malignant behavior of HCC cells and lead to abnormal mitochondrial function, thus playing the role of oncogene. MTFR2 is a mitochondrial regulatory factor and is connected to occurrence, development and unfavorable prognosis in cancer patients [11,12]. Lu et al documented elevated MTFR2 expression in breast cancer (BC) tissues, which was correlated with age, lymph node metastasis, HER2-positive status and unfavorable prognosis in BC patients [11].…”

“…Upregulated MTFR2 expression in oral squamous cell carcinoma tissues, abstracted from The Cancer Genome Atlas (TCGA) data resource and clinical tissue samples, is negatively linked to OS. MTFR2 can convert oxidative phosphorylation into glycolysis, thus promoting cancer cell growth and metastasis [12]. At present, there are few studies on MTFR2 in tumors, and its role and regulatory mechanism in most tumors, including HCC, are still a mystery.…”

Association of High Expression of Mitochondrial Fission Regulator 2 with Poor Survival of Patients with Esophageal Squamous Cell Carcinoma

“…Furthermore, it is involved in regulation of proliferation of glioma stem cells (GSCs) and thus may affect the prognosis of glioblastoma (9,17). Most recently, MTFR2 has been reported to promote the proliferation, migration, and invasion of oral squamous carcinoma (21), and MTFR2-dependent regulation of TTK was involved in maintaining GSCs in glioblastoma and might serve as a potential novel druggable target for glioblastoma. It might regulate the expression of TTK for participation in up-regulation and expression of GSCs in glioblastoma.…”