Fig. 5.

miR-16-5p served as tumor suppressor and reversed AGAP2-AS1 alteration mediated promotion of proliferation, migration, invasion and EMT in HCC. a HCCLM3 and Hep3B cells that were transfected with corresponding miRNA vectors were subjected to qRT-PCR for miR-16-5p expression. Overexpression of miR-16-5p inhibited cell proliferation (b), migration (c), invasion (d), EMT process (f) and promoted apoptosis (e) in HCCLM3 cells, while down-regulation of miR-16-5p promoted cell proliferation (b), migration (c), invasion (d), EMT process (f) and inhibited apoptosis (e) in Hep3B cells. g AGAP2-AS1-overexpressing Hep3B cells that were transfected with empty vector (miR-control) or miR-16-5p overexpression vector were subjected to qRT-PCR for miR-16-5p. AGAP2-AS1-suppressive HCCLM3 cells that were transfected with anti-miR-16-5p were subjected to qRT-PCR for miR-16-5p. miR-16-5p restoration abrogated the effects of AGAP2-AS1 overexpression on cell proliferation (h), migration (i), invasion (j), EMT process (l) and apoptosis (k) of Hep3B cells. miR-16-5p knockdown reversed the suppressive effects of AGAP2-AS1 knockdown in HCCLM3 cells (h-l). *P < 0.05, **P < 0.01