Mechanically, DLN did not function by reducing miR‑21 expression, whereas DLN and miR‑21 inhibitor downregulated B‑cell lymphoma-2 (BCL‑2) expression, and facilitated BCL‑2‑associated X protein (Bax) and P53 expression in melanoma cells.
Moreover, the expression level of Caspase 3 in lung tissues of rats in model group was significantly lower than that of miR-21 low-expression group, while the expression level of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (BAX) was markedly higher.
Furthermore, bioinformatics analysis indicated that programmed cell death 4 (PDCD4), phosphatase and tensin homolog deleted on chromosome ten (PTEN) and B‑cell lymphoma (Bcl)‑2 are potential target genes of miR‑21.
BISPR and miR-21-5p as well as B-cell lymphoma-2 (Bcl-2) expressions in TPC cells were determined by quantitative polymerase chain reaction (qRT-PCR) and Western blot.
Mechanistically, we discovered that knockdown of microRNA-21 increased programmed cell death protein 4 expression and nuclear factor-kappa B activity, decreased expression of anti-apoptotic B-cell lymphoma-2.
This study is to investigate the expression of miR-21 in nasopharyngeal carcinoma (NPC) cells, and the effect of miR-21 in the biological behavior and expression of B-cell lymphoma 2 (BCL2) in NPC cells.
During I/R and H/R, forced expression of miR-21 upregulated the Akt signaling activity via suppressing the expression of phosphatase and tensin homolog (PTEN) and the increased activity of Akt signaling further inhibited apoptosis partially by increasing the ratio of B-cell lymphoma 2(Bcl-2)/Bcl-2-associated X protein, which further suppressed the expression of caspase-3.