Overexpression of CFL1 in gastric cancer and the effects of its silencing by siRNA with a nanoparticle delivery system in the gastric cancer cell line.

Gastric adenocarcinoma, like other cancers, is a multifactorial genetic disease, and metastasis of cancer cells is one of the main features of this illness. The expression levels of the CFL1 gene have been modulated in this pathway. Using small interfering RNA (siRNA) in the treatment of gastric cancer is considered a hopeful gene therapeutic approach. The present study reported the level of CFL1 genes between tumor and margin and healthy tissue of gastric cancer. Also, the features of a cationic nanoparticle with a polymer coating containing polyacrylic acid and polyethyleneimine that were used in the delivery of CFL1 siRNA, were shown. Then the cytotoxicity, cellular uptake, and gene silencing efficiency of this nanoparticle were evaluated with CFL1siRNA. METHOD:In this study, the CFL1 gene expression was measured in 40 gastric adenocarcinoma, marginal and 15 healthy biopsy samples by a real-time polymerase chain reaction. Physicochemical characteristics, apoptosis, and inhibition of migration of the delivery of CFL1 siRNA by nanoparticle and lipofectamine were investigated in gastric cancer cells. RESULT:The CFL1 expression was remarkably increased in gastric cancer tissues in comparison with the marginal samples and normal tissues (p < .05) and the biomarker index for CFL1 was obtained as 0.94, then this gene can be probably used as a biomarker for gastric cancer. After treatment of the AGS cell line by CFL1 siRNA, the CFL1 expression level of mRNA and migration in AGS cells were remarkably suppressed after transfection. Furthermore, the amount of apoptosis increased (p < .05). CONCLUSION:Our results demonstrated that CFL1 downregulation in AGS cells can interdict cell migration. Finally, our outcomes propose that CFL1 can function as an oncogenic gene in gastric cancer and would be considered as a potential purpose of gene therapy for gastric cancer treatment.

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