Histamine modulates cellular events involved in tumour invasiveness in pancreatic carcinoma cells

G. CRICCO; M. NÚÑEZ; V. MEDINA; G. GARBARINO; N. MOHAMAD; A. GUTIÉRREZ; C. COCCA; R. BERGOC; E. RIVERA; G. MARTÍN

Inflammation Research

Año: 2006 vol. 55 p. 83 - 84

Progression of epithelial tumours to metastatic stage is characterized by increased motility, decrease in cellular adhesion, high expression and activation of metalloproteases (MMPs) and high angiogenic capability. Pancreatic adenocarcinoma is highly aggressive malignant tumour which rapidly progresses. Previously we have reported human pancreatic adenocarcinoma cell line PANC-1 overexpresses H1 and H2 histamine receptors. These cells synthesize and secrete histamine (HA) to the extracellular medium where it acts as a growth factor modulating cellular proliferation via H1 and H2 histamine receptors. Thus HA on cellular adhesion and migration plus the role of MMPs in the invasive potential of this cell line was studied. The downregulation of adhesion molecules promote cell disagregation whereas MMPs facilitate cell migration. Diminution in cellular adhesion observed in PANC-1 cells treated with HA, H1 agonist, H1 orH2 antagonist could be related to increase of MMP-2 gelatinolytic activity. We propose that HA may play a crucial role in tumoural progression towards metastasis in pancreatic carcinoma cells.