Abstract

BackgroundWe aimed to determine the SSRP1's potential influence on the apoptosis and proliferation of gastric cancer (GC) cells and its regulatory mechanism.MethodsSSRP1 expression in GC cells and tissues was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The interrelation between clinicopathological characteristics of GC patients and SSRP1 expression was analysed via x2 test, and the correlation between SSRP1 expression and overall survival rate was analysed using Kaplan-Meier survival analysis. After the knockdown of SSRP1 in AGS cells, the SSRP1 expression, colony formation ability, cell viability, cell cycle changes, apoptosis rate, and migration and invasion ability were detected through qRT-PCR, colony formation assay, CCK8 assay, flow cytometry and transwell test, respectively. Finally, the effects of down-regulation of SSRP1 on the expressions of phosphorylated-protein kinase B (p-AKT), B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) were explored using Western blotting.ResultsSSRP1 displayed a high expression in GC cells and tissues. SSRP1 expression was closely interrelated to the TNM stage, lymph node metastasis and tumour size. The survival rate of patients was markedly shorter in the high expression group than in the lower expression group. After the knockdown of SSRP1 in cells, the viability and colony formation ability of AGS cells were inhibited. In addition, the cell ratio in the G1 phase was increased, while that in the S phase declined, and the cell invasion and migration were obviously weakened. It was found from Western blotting that the knockdown of SSRP1 could evidently suppress the protein levels of Bcl-2 and p-AKT but promote the protein expression of Bax, indicating that silencing SSRP1 can inhibit the proliferative capacity and increase the number of GC cells through inactivating the AKT signalling pathway.ConclusionsSSRP1 rose up in GC tissues and cells. Reduction of SSRP1 can inhibit the proliferative capacity and increase the number of GC cells through inactivating the AKT signalling pathway.

Highlights

  • Gastric cancer (GC) is a frequently seen malignancy seriously threatening human health

  • It was discovered that Structure-specific recognition protein 1 (SSRP1) expression rose in GC cell lines, and it showed the highest value in AGS cell lines, so AGS cell lines were selected for subsequent knockdown assay (Figure 1B)

  • The results revealed that the patients in the high-expression group displayed a larger tumour size and advanced TNM stage, and are often accompanied by lymph node metastasis, showing statistically significant differences (P

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Summary

Introduction

Gastric cancer (GC) is a frequently seen malignancy seriously threatening human health. The 5year survival rate of GC patients in China has dramatically risen with the early gastroscopy and prompt surgical intervention in recent years [3]. The 5-year survival rate of advanced GC remains low [4]. Structure-specific recognition protein 1 (SSRP1) was originally identified as a high-mobility group 1 (HMG1)-related DNA-binding protein in 1991, and its biological functions can be attributed to its HMG domain [5]. It is believed that SSRP1 dramatically influences the development and occurrence of tumours, and its expression is upregulated in such tumours as hepatocellular cancer [10], colorectal cancer [11], nasopharyngeal cancer [12] and glioma [13]. The biological role and mechanism of SSRP1 in gastric cancers remain unclear

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