The silencing of FGFR2 was demonstrated to augment the effects of cisplatin treatment, including decreasing the cell viability and inducing cell cycle arrest, which involved the increase and decrease of the durations of G1 and S phases, respectively, and a decrease in the expression levels of cyclin D1 and CDC25A, and increasing the rate of apoptosis via the intrinsic apoptosis pathway, as demonstrated by the upregulation of cleaved caspase‑3 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein and downregulation of Bcl‑2, in SUNE1 and C666‑1 cell lines.
The effects of miR‑181a on cell division cycle 25A (CDC25A), cyclin A2, cyclin D1, p21, Bcl‑2‑associated X protein (Bax) and B‑cell lymphoma‑2 (Bcl‑2) protein levels were assessed in gastric cancer cell lines. miR‑181a directly interacted with the 3'‑untranslated region of RASSF1A and downregulated RASSF1A protein expression.
Furthermore, downregulation of mitochondrial membrane potential, B-cell lymphoma-2 (BCL-2) and CDC25A, as well as upregulation of BCL-2‑associated X protein (Bax) and caspase-3 expression in Art-treated cells were identified.
We evaluated Cdc25A mRNA expression by in situ hybridization and p27 protein expression by immunohistochemistry in 42 histologically indolent B-cell non-Hodgkin lymphoma (NHL and 51 histologically aggressive B-cell NHL.