We found that ectopic expression of gga-miR-16-5p in DF-1 cells enhanced IBDV-induced apoptosis by directly targeting cellular anti-apoptotic protein B-cell lymphoma-2 (Bcl-2), facilitating IBDV replication in DF-1 cells.
Additionally, in hypoxic/SD conditions, miR‑16 expression increased and B‑cell lymphoma (Bcl)‑2 protein expression decreased in BM‑MSCs. miR‑16 did not affect Bcl‑2 mRNA expression but downregulated Bcl‑2 protein expression. miR‑16 inhibitor transfection significantly increased Bcl‑2 protein expression and the percentage of apoptotic BM‑MSCs was reduced.
SERT, B‑cell lymphoma‑2 (Bcl‑2) and brain derived neurotropic factor (BDNF) expression levels were evaluated by western blotting, and miR‑16 expression was evaluated by reverse transcription‑quantitative polymerase chain reaction.
Two miRNAs, hsa-miR-17-5p and hsa-miR-16-5p, were identified as having the highest associations with targeted mRNAs [such as B-cell lymphoma 2 (BCL2), small body size/mothers against decapentaplegic 3 (SMAD3) and suppressor of cytokine signaling 1 (SOCS1)] and pathways associated with epithelial-mesenchymal transitions and other processes linked with cancer metastasis (including cell cycle, adherence junctions and extracellular matrix-receptor interaction). mRNAs for two genes [HECT, UBA and WWE domain containing 1 (HUWE1) and BCL2] were found to have the highest associations with miRNAs, which were down-regulated in brain metastasis specimens of breast cancer.