RESUMO
PURPOSE: To explore whether miR-573 can suppress pancreatic cancer cell proliferation, migration, and invasion by targeting TSPAN1. METHODS: The expression of miR-573 and TSPAN1 in pancreatic cancer tissues and cells lines was analyzed using RT-qPCR. The human pancreatic cancer cell line PANC1 was transfected with miR-573 mimic, pcDNA3.1-TSPAN1, or genOFFTM st-h-TSPAN1. The effects of miR-573 and TSPAN1 on cell proliferation, colony formation, migration, and invasion were analyzed by CCK8, colony formation, transwell migration, and invasion assay, respectively. Target genes of miR-573 were screened using bioinformatics tools and confirmed by dual-luciferase reporter assay and real-time PCR. The effects of miR-573 in vivo were observed using tumor xenografts. RESULTS: We found that miR-573 is downregulated and TSPAN1 is upregulated in pancreatic cancer tissues and cells lines. Function assays demonstrated that overexpression of miR-573 inhibited cell proliferation, colony formation, migration, and invasion of pancreatic cancer cells, as well as suppressing tumor growth in vivo. Target genes of miR-573 were predicted using bioinformatics tools and confirmed by dual-luciferase reporter assay and RT-qPCR or western blotting. Downregulation of TSPAN1 also inhibited cell proliferation, colony formation, migration, and invasion of pancreatic cancer cells. Furthermore, overexpression of TSPAN1 attenuated miR-573-induced inhibition of pancreatic cancer cell proliferation and migration. CONCLUSION: Our findings indicated that miR-573 suppresses pancreatic cancer cell proliferation, migration, and invasion through targeting TSPAN1. TSPAN1 targeted by miR-573 might be a potential therapeutic target for clinical treatment of pancreatic cancer.
Assuntos
MicroRNAs/fisiologia , Proteínas de Neoplasias/antagonistas & inibidores , Neoplasias Pancreáticas/patologia , RNA Neoplásico/fisiologia , Tetraspaninas/antagonistas & inibidores , Animais , Divisão Celular , Linhagem Celular Tumoral , Movimento Celular , Regulação para Baixo , Regulação Neoplásica da Expressão Gênica/genética , Genes Reporter , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/biossíntese , MicroRNAs/genética , MicroRNAs/uso terapêutico , Invasividade Neoplásica , Proteínas de Neoplasias/biossíntese , Proteínas de Neoplasias/genética , RNA Neoplásico/biossíntese , RNA Neoplásico/genética , Distribuição Aleatória , Reação em Cadeia da Polimerase em Tempo Real , Organismos Livres de Patógenos Específicos , Tetraspaninas/biossíntese , Tetraspaninas/genética , Ensaio Tumoral de Célula-Tronco , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
The overdosage use of pesticide was harmful to the environment and human health, which was mainly caused by the low utilization rate of the pesticide. However, the pesticide microcapsule with sustained-release and stimulating response properties could effectively solve this problem. Preparation of carboxymethyl cellulose grafting dimethyldiallylammonium chloride (CMC-g-PDMDAAC) through grafting polymerization and trapping as well as encapsulation of avermectin (AVM) via electrostatic interactions resulted in the formation of AVM/CMC-g-PDMDAAC microcapsules. The results showed that the particle size was 200~300 nm. The encapsulation efficiency was as high as 72.06%. Furthermore, the remaining rate of encapsulated AVM increased from 50.0 to 81.60% after UV irradiation for 359 min. The microcapsules exhibited significant enzyme and pH stimuli responsiveness. Finally, CMC-g-PDMDAAC had no significant difference effect on the toxicity of AVM, AVM could be found, and DMDAAC featured a synergistic effect on the toxicological effects of AVM. Graphical abstract.
