In preclinical models, tumor cell PAR-1 appeared to be involved in the regulation of lung tumor growth and metastasis; however the role of PAR-1 in the lung tumor microenvironment, which is emerging as a key compartment in driving cancer progression, remained to be explored.
Comparable in efficacy with Bevacizumab, monotherapy with the PAR1 i3 loop pepducin P1pal-7 provided significant 75% inhibition of lung tumor growth in nude mice.
More recently, we mapped additional lung tumor resistance loci (Par2, and Par4), and a locus specifically involved with lung tumor progression (Papg1).
Thus, in this study we found no evidence that either Smad4 or Smad2 represents the Par2lung tumor resistance locus or is a lung tumor suppressor gene in the B6CF1 mice.