Research Paper Volume 12, Issue 18 pp 18019—18032

Figure 5. Downregulation of miR-424-5p partly rescues si-AGAP2-AS1 mediated inhibition of invasion and migration in PTC cells. (A, B) Trans-well assays of PTC cell migration and invasion after transfection with si-AGAP2-AS1, or a co-transfection with miR-424-5p inhibitor and si-AGAP2-AS1 or NC. Data are presented as the mean ± S.D., analyzed using an independent samples t-test; **P < 0.01 vs. the si-AGAP2-AS1 group. (C, D) Wound-healing assay of PTC cell migration and invasion after transfection with si-AGAP2-AS1, or co-transfection with miR-424-5p inhibitor and si-AGAP2-AS1 or NC. (E) Western blotting of MMP2 after transfection with si-AGAP2-AS1 or co-transfection with miR-424-5p inhibitor and si-AGAP2-AS1 or NC. Data are presented as the mean ± S.D., analyzed using an independent samples t-test; **P < 0.01 vs. the si-AGAP2-AS1 group. (F) Schematic illustration of the proposed function of AGAP2-AS1 in PTC. AGAP2-AS1 functions as a competing endogenous RNA that upregulates MMP2 expression and promotes PTC progression by sponging miR-424-5p. (G) AGAP2-AS1 played a role as ceRNA in different cancers.