Abstract

BackgroundOral squamous cell carcinoma (OSCC) is one of the most common types of malignancy. Semaphorin 3F (SEMA3F) is highly conserved but present at a lower level in various cancers than in healthy tissues. While it has been reported that SEMA3F is involved in cancer cell proliferation, migration and invasion, its function in OSCC remains unknown.MethodsThe expression of SEMA3F in OSCC tissues and OSCC-derived cells was analyzed using qRT-PCR and western blotting. Using SAS and HSC2 cells, we also monitored the effect of SEMA3F on OSCC cell proliferation, migration and invasion using MTT, colony formation and transwell assays. The function of SEMA3F in OSCC tumor formation was also assessed in vivo.ResultsSEMA3F was significantly downregulated in OSCC tissues and OSCC-derived cells. SEMA3F shows growth inhibitory activity in SAS and HSC2 cells and may act as a tumor suppressor. It can inhibit the migration and invasion potential of OSCC cells. Our results also demonstrate that SEMA3F can suppress the growth of OSCC cells in vivo.ConclusionsThis study revealed that SEMA3F plays a role as a tumor suppressor in OSCC cell proliferation, migration and invasion. Our finding provides new insight into the progression of OSCC. Therapeutically, SEMA3F has some potential as a target for OSCC treatment, given sufficient future research.

Highlights

  • Oral squamous cell carcinoma (OSCC) is one of the most common types of malignancy

  • This study revealed that Semaphorin 3F (SEMA3F) plays a role as a tumor suppressor in OSCC cell proliferation, migration and invasion

  • Expression of SEMA3F in oral cancer tissue samples and cells To identify the role of SEMA3F in oral carcinogenesis, we tested the expression levels of SEMA3F in a cohort of OSCC tissues and adjacent normal tissues using quantitative reverse transcription PCR (qRT-PCR)

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Summary

Introduction

Oral squamous cell carcinoma (OSCC) is one of the most common types of malignancy. While it has been reported that SEMA3F is involved in cancer cell proliferation, migration and invasion, its function in OSCC remains unknown. Oral squamous cell carcinoma (OSCC) is the most common malignant neoplasm of the oral cavity [1, 2]. According to the recent investigation of its pathogenesis and management, OSCC affects approximately 300,000 individuals per year worldwide, and the five-year survival rate for patients remains as low as 60% [3,4,5]. Recent investigations of molecular alterations in various oncogenes and antitumor genes associated with OSCC development may help to address this [3, 11, 12].

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