Title : pERK1/2 silencing sensitizes pancreatic cancer BXPC-3 cell to gemcitabine-induced apoptosis via regulating Bax and Bcl-2 expression.

Pub. Date : 2015 Feb 21

PMID : 25880226






7 Functional Relationships(s)
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1 pERK1/2 silencing sensitizes pancreatic cancer BXPC-3 cell to gemcitabine-induced apoptosis via regulating Bax and Bcl-2 expression. gemcitabine BCL2 associated X, apoptosis regulator Homo sapiens
2 It has also shown that Bcl-2 confers resistance and Bax sensitizes to gemcitabine-induced apoptosis in pancreatic cancer cells. gemcitabine BCL2 associated X, apoptosis regulator Homo sapiens
3 We therefore tested the hypothesis that pancreatic cancer cells are resistant to gemcitabine and this resistance is due to activation of ERK1/2 and subsequent upregulation of Bcl-2 and downregulation of Bax. gemcitabine BCL2 associated X, apoptosis regulator Homo sapiens
4 Combined treatment with PD98059 and Bax siRNA transfection could decrease gemcitabine-induced ERK1/2 and Bax activation, which subsequently resulted in decreased apoptosis. gemcitabine BCL2 associated X, apoptosis regulator Homo sapiens
5 Combined treatment with PD98059 and Bax siRNA transfection could decrease gemcitabine-induced ERK1/2 and Bax activation, which subsequently resulted in decreased apoptosis. gemcitabine BCL2 associated X, apoptosis regulator Homo sapiens
6 CONCLUSIONS: The upregulation of ERK1/2-dependent Bcl-2 and downregulation of ERK1/2-dependent Bax can protect human pancreatic cancer cells from gemcitabine-induced apoptosis. gemcitabine BCL2 associated X, apoptosis regulator Homo sapiens
7 Targeting the ERK1/2-Bax/Bcl-2 pathway may in part lead to sensitization of pancreatic cancer to gemcitabine. gemcitabine BCL2 associated X, apoptosis regulator Homo sapiens