Mechanism research on Long noncoding RNA (lncRNA) GASL1 carried with lipid nanoparticles in restraining cervical carcinoma transplantable tumor through targeting of miR-21 and induction of STAT3/survivin signal channel

Abstract

This study assessed the mechanism of lncRNA-GASL1 carried with lipid nanoparticles in restraining cervical carcinoma transplantable tumor through targeting miR-21 and inducing the STAT3/Survivin signal channel. 50 rats were randomly divided into control set, model set, GASL1 set, miR-21mimic set and agonist set. There were ten rats in every set. Expression of lncRNA-GASL1, anti-tumor rate, thymus index, spleen index, and protein expression of MIF, VEGF-C and p53 were studied, including protein expression of factors related with STAT3/Survivin signal transduction pathway, miR-21 presentation, targeting correlation between lncRNA-GASL1 and miR-21 were all observed. Expressions of lncRNA-GASL1 in the model set and agonist set were lower than in the other sets. The second highest expression was in the miR-21mimic set, where it was increased notably in the GASL1 set. The expression was highest in the control set. The thymus index and spleen index in the control set was highest. The expressions of miR-21mimic set and GASL1 set were increased notably and anti-tumor rate was reversed. There was no apoptosis in the control set, while there was lower quantity of apoptotic cells in the model and agonist sets. The inhibitor action of lncRNA-GASL1 on the transplantable tumor in cervical carcinoma was related with STAT3/Survivin signal transduction pathway, while there was lncRNA-GASL1 targeting combined with miR-21. The miR-21 presentation was reduced, while activity of STAT3 as target gene for miR-21 was reduced. The STAT3 was phosphorylated, while activity of Survivin was reduced. The phosphorylation level of Survivin was reduced, while growth of transplantable tumor in cervical carcinoma was restrained.