Abstract:
OBJECTIVES:Protein kinase C (PKC) is involved in tumor growth and apoptosis and hence represents a potential target for cancer therapy. This study investigated the expression of PKC in pancreatic tumor tissue in comparison to adjacent normal tissue and determined the modulation of PKC by bryostatin-1 (BRYO) on pancreatic cancer cell lines. METHODS:Pancreatic tissue was obtained from 18 patients who had a resection (14 with ductal adenocarcinoma and 4 with adenoma and high-grade dysplasia). Cytosolic and nuclear membrane PKCs in the paired samples were determined by immunoblotting. HPAC cells were treated with gemcitabine and BRYO and in sequential and concomitant combination. To evaluate cell viability, apoptosis, and electrophoretic mobility shift assay, 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, enzyme-linked immunosorbent assay, and nuclear factor kappaB (NF-kappaB) assays were used. RESULTS:As compared with the adjacent normal tissue, PKC-alpha, PKC-beta1, and PKC-delta were higher in the tumor; PKC-epsilon was higher in the normal tissue. Pretreatment with gemcitabine followed by BRYO resulted in decreased cell viability, increased apoptosis, and inhibited NF-kappaB than either agent alone or BRYO followed by gemcitabine. CONCLUSION:Protein kinase C is overexpressed and activated in pancreatic cancer as compared with normal tissue. Inhibition of PKC could sensitize pancreatic cancer cell lines to the effects of gemcitabine. The potentiation of gemcitabine by BRYO is sequence-dependent and mediated through inhibition of PKC-dependent activation of NF-kappaB.
journal_name
Pancreasjournal_title
Pancreasauthors
El-Rayes BF,Ali S,Philip PA,Sarkar FHdoi
10.1097/MPA.0b013e31815ceaf7subject
Has Abstractpub_date
2008-05-01 00:00:00pages
346-52issue
4eissn
0885-3177issn
1536-4828pii
00006676-200805000-00004journal_volume
36pub_type
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