JWA gene regulates PANC-1 pancreatic cancer cell behaviors through MEK-ERK1/2 of the MAPK signaling pathway
- Authors:
- Published online on: July 9, 2014 https://doi.org/10.3892/ol.2014.2329
- Pages: 1859-1863
Metrics: Total
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
Abstract
The present study aimed to investigate the role of JWA gene in the proliferation, apoptosis, invasion and migration of PANC‑1 pancreatic cancer cells and the effect on the MAPK signaling pathway. Human PANC‑1 pancreatic cancer cells were cultured in vitro, and small interfering RNA (siRNA) was designed for the JWA gene. The siRNA was transfected into PANC‑1 cells. Subsequently, the cell proliferation was measured by MTT assay; cell apoptosis was detected by analyzing BAX and Bcl‑2 protein expression; cell migration and invasion were measured using Transwell® chambers; and the protein expression of JWA and ERK1/2, JNK and p38 and their phosphorylated forms were measured by western blotting. By utilizing the MTT assay, the results showed that when JWA protein expression was inhibited, the proliferation of PANC‑1 cells was enhanced. In addition, the expression of apoptosis‑associated protein (AAP) BAX was substantially decreased, while the expression of the apoptosis inhibitor gene, Bcl‑2, was significantly enhanced. Using Transwell chambers, it was found that the number of penetrating PANC‑1 cells was significantly increased after transfection with JWA siRNA, suggesting that the migration and invasion of the cells was substantially increased. By studying the association between JWA and the MAPK pathway in PANC‑1 cells, it was found that the expression of p‑ERK1/2 of the MAPK pathway was significantly downregulated following JWA siRNA transfection. However, the expression levels of ERK1/2, JNK, p38, p‑JNK and p‑p38 showed no significant differences. In conclusion, it was shown that JWA affects the proliferation, apoptosis, invasion and migration of PANC‑1 pancreatic cancer cells which could be attributed to effects on the expression of ERK1/2 in the MAPK pathway.
