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.
Highlights
Oral squamous cell carcinoma (OSCC) is the most common type of cancer in the head and neck area
Cancer cells tend to degrade glucose to lactic acid even in an environment supplied with oxygen, which is known as glycolysis [5]
We scanned the TCGA database and identified that MTFR2 was upregulated in OSCC
Summary
Oral squamous cell carcinoma (OSCC) is the most common type of cancer in the head and neck area. It is one of the ten most common cancers and is listed as the most common malignancy in the Department of Oral and Maxillofacial Surgery [1]. Glycolysis is one of the metabolic hallmarks of cancer cells. Cancer cells tend to degrade glucose to lactic acid even in an environment supplied with oxygen, which is known as glycolysis [5]. We detected the OCAR and ECAR and the markers of OXPHOS and glycolysis, this result revealed that MTFR2 promotes proliferation, migration and invasion in oral squamous carcinoma cell lines by switching OXPHOS to glycolysis
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.