Abstract

BackgroundTo investigate the expression of RASSF-1A in oral squamous cell carcinoma (OSCC) and adjacent tissues, and to explore its mechanism of action in the development of OSCC.MethodsRASSF-1A and proliferation-related protein expression in clinical and OSCC mouse models were detected by qPCR and western blot. In vitro experiments were used siRNA knockdown of RASSF-1A gene in SCC9 cells to detect cell proliferation, migration and apoptosis. In vivo experiments were performed using adenovirus overexpressing RASSF-1A gene in mice and observing tumor growth.ResultsThe results of qPCR and western blot showed that the expression of RASSF-1A gene was decreased in OSCC, and the expression of CyclinD1 protein was increased. The results of co-immunoprecipitation showed that the two proteins were significantly combined in the oral cancer cell line. Knocking down the RASSF-1A gene in SCC9 cells promotes cell migration and proliferation, while reducing apoptosis and increasing CyclinD1 protein expression. Overexpression of RASSF-1A gene in mice reduces tumor volume and inhibits CyclinD1 protein expression.ConclusionsLow expression of RASSF-1A gene in OSCC promotes the expression of CyclinD1 protein and tumor growth.

Highlights

  • To investigate the expression of RASSF-1A in oral squamous cell carcinoma (OSCC) and adjacent tissues, and to explore its mechanism of action in the development of OSCC

  • Low expression of RASSF‐1A in tumor tissues of patients with oral squamous cell carcinoma In order to observe the expression of RASSF-1A gene in OSCC, we collected 6 tumors and adjacent tissues from patients with clinical OSCC and extracted tissue RNA and whole protein

  • Flow cytometry showed that the percentage of cells knocking down the RASSF-1A gene in the S phase was significantly higher than that in the control group, indicating that the proliferation of SCC9 cells was significantly increased after knocking down the gene (Fig. 2d)

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Summary

Introduction

To investigate the expression of RASSF-1A in oral squamous cell carcinoma (OSCC) and adjacent tissues, and to explore its mechanism of action in the development of OSCC. Oral cancer is one of the ten most common malignant tumors in the world, accounting for 5% of systemic malignancies, 90% of which are epithelial-derived squamous cell carcinoma [1]. The incidence of oral squamous cell carcinoma (OSCC) is increasing and the age of onset is getting younger [2]. Quamous cell carcinoma, abbreviated as squamous cell carcinoma, known as epidermal carcinoma, is a malignant tumor that occurs in the epidermis or accessory cells. The cancer cells have different degrees of keratinization, and are more common in areas covered with squamous epithelium, such as skin, mouth, lips, esophagus, cervix, vagina, etc. The World Health Organization predicts that the incidence of OSCC will continue to rise in

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