RESUMEN
Gastric cancer is one of the most common cancers globally with high rates of morbidity and mortality. Purified Omphalia lapidescens protein (pPeOp) is a protein extracted from the sclerotium of Omphalia lapidescens. The present study aimed to investigate the effects of pPeOp on the viability, migration, cell cycle progression and apoptosis of SGC-7901 cells. The expression of numerous proteins, namely matrix metallopeptidase (MMP)2, MMP9, p53, caspase-3, B-cell lymphoma (Bcl)-2, cyclin A2, cyclin B1, cyclin D1, cyclin dependent kinase (CDK)1, CDK2 and CDK4, were investigated using western blot analysis and reverse transcription-quantitative polymerase chain reaction. The results of the present study demonstrated that treating SGC-7901 cells with pPeOp markedly suppressed their migration, induced their apoptosis and arrested their progression in S phase. pPeOp also downregulated the expression of migration-associated proteins (MMP2 and MMP9) and cyclin-associated proteins (cyclin A2, cyclin B1, cyclin D1, CDK1, CDK2 and CDK4) in a dose-dependent manner. Cells treated with pPeOp significantly upregulated caspase-3 and p53 and downregulated Bcl-2. Finally, the impact of pPeOp on three key nodes of the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway were investigated and it was revealed that expression levels of JAK1, JAK2 and STAT3 were significantly downregulated following treatment. Together, the results of the present study suggested that pPeOp suppresses metastasis, arrests cell cycle, induces apoptosis and inhibits the JAK-STAT signaling pathway in SGC-7901 cells. Therefore, pPeOp may serve as a novel therapeutic agent for patients with gastric cancer.
RESUMEN
The aim of the present study was to investigate the effect of purified Omphalia lapidescens protein (pPeOp) extracted by polyvinylpyrrolidone from the fungus Omphalia lapidescens Schroet on the proliferation and cell cycle progression of MC-4 human gastric tumor cells. Using polyvinylpyrrolidone, pPeOp was extracted from O. lapidescens Schroet. MC-4 cells were cultured with 30, 60 or 90 µg/ml pPeOp, with 5-fluorouracil used as a positive control. Survival rates of treated cells were significantly decreased compared with those of the untreated control group in a dose-dependent manner. Using flow cytometric analysis, cells treated with pPeOp were demonstrated to arrest in S phase and exhibit abnormal G0/G1 and G2/M phase cell cycle distribution. In addition, a wound healing assay demonstrated that pPeOp significantly inhibited the migration of MC-4 cells. The mRNA and protein expression levels of cyclin D1/cyclin-dependent kinase (CDK) 4, cyclin B/CDK1, cyclin A/CDK2, matrix metalloproteinase (MMP)-2 and MMP-9 were determined using reverse transcription-quantitative polymerase chain reaction analysis and western blotting. The mRNA expression level of CDK4 and cyclin A was significantly increased compared with the untreated control; however, cyclin D1, CDK1, CDK2, cyclin B, MMP-2, and MMP-9 exhibited a significantly decreased mRNA expression level, indicating that there is a negative association between concentration and cyclin D1 expression levels. The expression of the cycle arrest-associated proteins and migration-associated proteins examined were similar to the observed mRNA expression levels. In conclusion, pPeOp was identified to inhibit migration of and cause S phase cell cycle arrest in MC-4 cells.