Conclusion
HnRNP D was associated with resistance to GEM in pancreatic cancer cells. Decreasing of hnRNP D expression promoted cell apoptosis induced by GEM.
Methods
The expressions of hnRNP D in clinical pancreatic cancer tissues were detected by immunohistochemistry. The proliferation of pancreatic cancer cell lines (PANC-1, BXPC-3, SW1990 and ASPC-1) were measured by CCK8 assay. IC50 of each cell line was calculated and compared. The expressions of hnRNP D protein in pancreatic cancer cell lines were detected by Western Blot assay. The change of hnRNP D expression was confirmed by qPCR and Western Blot after the expressions of hnRNP D in PANC-1 cells being down-regulated by miRNA. And than the apoptosis rate and cell cycle of PANC-1 cells were detected by flow cytometry, while the expressions of apoptosis-related proteins cleaved caspase3, P-Akt, AKT and P65 were detected by Western Blot.
Objective
To investigate the role of ribosomal associated protein hnRNP D in resistance to gemcitabine (GEM) in pancreatic cancer cells.
Results
HnRNP D protein expressed in clinical pancreatic tissues widely. The IC50 of GEM in PANC-1 was the highest while in BXPC-3 was the lowest. And the expression of hnRNP D protein in PANC-1 was the highest while in BXPC-3 was the lowest. After miRNA interfering, the expressions of hnRNP D protein and gene were significantly decreased in PANC-1 cells. The decrease of hnRNP D expression promoted cell apoptosis and inhibited the cell transformation to the S phase in cell cycle. Under the intervention of GEM, cleaved caspase3 expression was significantly increased, while p-Akt, AKT and P65 expression was significantly decreased.