Oral Presentation 6th Australian Health and Medical Research Congress 2012

Influence of Apolipoprotein A-II in Pancreatic Cancer Cell Proliferation (#202)

Senthil Supramaniam 1 , Aiqun Xue 1 , Thao Nguyen 1 , Ross Smith 1
  1. Kolling Institute of Medical Research, St Leonards, NSW, Australia


To evaluate the effects of lipids on promotion of pancreatic cancer cells mitogenesis and to determine uptake of Apoprotein A-II (Apo A-II) by pancreatic cancer.


Pancreatic cancer is the 4th leading cause of cancer death in the world with a 5 year overall survival of less than 5%. Many patients present with advanced disease, making only 30% of patients suitable for surgery. Despite aggressive surgery, the prognosis remains dismal. CA 19.9 is usually detected when tumour is large and CEA has a poor sensitivity to pancreatic cancer. Hence, the need for a reliable pancreatic cancer biomarker is paramount.


In vitro experimental studies were conducted using pancreatic cancer lines (CFPAC-1, PANC-1 and CAPAN-2) which were treated with various combinations of lipids and Apolipoprotein A-II (Apo A-II). Apo A-II was also labeled with antibodies for the purpose of determining their intracellular location using confocal fluorescence microscopy. Cell proliferation activity was determined for these cell lines using crystal violet assay.


The three cell lines displayed different trends of cell growth i.e. growth increased over time for CFPAC-1 and PANC-1 and not in order in CAPAN-2 whereby increased mitogenesis was noticed in the control group. The variability in result demonstrated the heterogeneity in pancreatic tumor and their biological behaviour. Confocal fluorescence microscopy also confirmed cystosolic presence of Apo A-II in pancreatic cancer cells.


Lipids have a mitogenic effect of pancreatic cancer cell proliferation, which is in accordance with literature, however their effect is enhanced by Apo A-II. This was further supported by localization of Apo A-II in cell cystosol in the setting of lipid treatment. Cells treated with Apo A-II alone did not show intracellular Apo A-II. This study paves way for future research into role of Apo A-II as a potential biomarker for pancreatic cancer. This study should also be advanced into in vivo models to examine uptake of ApoA-II by pancreatic cancer.