Directed antisense therapy confirms the role of protein kinase C-alpha in the tumorigenicity of pancreatic cancer

Surgery. 1998 Aug;124(2):218-23; discussion 223-4.

Abstract

Background: The level of expression of the alpha isoform of protein kinase C (PKC-alpha) has been shown to correlate inversely with the pathologic differentiation of human pancreatic cancers.

Methods: We stably transfected a moderately differentiated pancreatic cell line (HPAC) to overexpress PKC-alpha and examined the survival rates compared with parent HPAC according to an orthotopic model. Next we used a PKC-alpha antisense oligonucleotide specifically to down-regulate this isoform in vitro and examine the effect of treatment in vivo again according to the orthotopic model.

Results: Animals implanted with the overexpressing cell line had a mortality rate almost twice that of those implanted with the parent cell line (P < .01). Treatment with antisense oligonucleotide in increasing concentrations down-regulated PKC-alpha mRNA by Northern blot analysis and reverse transcriptase-polymerase chain reaction. Animals treated with antisense oligonucleotide after orthotopic implantation of pancreatic cancer cells survived statistically longer than those treated with vehicle alone (P = .005). Treatment with a scrambled oligonucleotide also conferred a survival benefit compared with vehicle alone (P < .01).

Conclusions: Tumorigenicity of pancreatic cancer is related directly to PKC-alpha expression in vivo as demonstrated by decreased survival when overexpressed. PKC-alpha expression can be down-regulated directly (antisense) and indirectly (scrambled) in vitro, which subsequently confers a dramatic survival benefit in vivo.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adenocarcinoma / metabolism
  • Adenocarcinoma / mortality
  • Adenocarcinoma / therapy*
  • Animals
  • Carcinogenicity Tests
  • DNA, Antisense / pharmacology
  • DNA, Complementary / pharmacology
  • Disease Models, Animal
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Regulation, Neoplastic
  • Genetic Therapy*
  • Humans
  • Isoenzymes / genetics*
  • Isoenzymes / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / mortality
  • Pancreatic Neoplasms / therapy*
  • Protein Kinase C / genetics*
  • Protein Kinase C / metabolism
  • Protein Kinase C-alpha
  • RNA, Messenger / genetics
  • Survival Analysis
  • Tumor Cells, Cultured / enzymology

Substances

  • DNA, Antisense
  • DNA, Complementary
  • Isoenzymes
  • RNA, Messenger
  • PRKCA protein, human
  • Prkca protein, mouse
  • Protein Kinase C
  • Protein Kinase C-alpha