Our study assessed mechanism of miR-21 antagonist packaged with arsenic trioxide nanoparticles (As2O3) in restraining invasion and metastasis of intestinal cancer by targeted CCR7 protein through induction of PI3K/Akt signal pathway. SW480 cell strains were adopted
and divided into blank group, group with empty carrier, group with miR-21 agonist and group with miR-21 antagonist packaged with nanoparticles. Cell invasion and metastasis was observed after they were interfered with miR-21 agonist. Expressions of N-cadherin, Vimentin, MMP-9, MMP-2, PI3K
and Akt were detected and targeted correlation between miR-21 and CCR7 was studied. The quantity of cells cross matrix membrane in group with carrier and miR-21 antagonist was lowest, while the quantity in the agonist group was highest. The expressions of N-cadherin, Vimentin, MMP-9, MMP-2,
PI3K and Akt in group with carrier and antagonist were lower than in the other three groups, and expression of-cadherin and CCR-7 was reversed. The expression of CCR7 was up-regulated by the miR-21 antagonist packaged with nanoparticles, while activated degree of PI3K/Akt was restrained. The
level of pathway factor was reduced abnormally so as to regulate the EMT procession, and expression of E-cadherin was increased. Moreover, the expression of MMP-9 and MMP-2 was reduced, and cell invasion and metastasis were controlled. The molecular mechanism was related with PI3K/AKt signal
pathway.