Neutralisation of gastrin in the INS-GAS mouse model reduced expression of MMP-7, HB-EGF and key EMT proteins.
Neutralisation of gastrin in an INS-GAS mouse in vivo carcinogenesis model leads to reduced proliferation and MMP-7, Slug and HB-EGF expression.
Finally, the involvement of the gastrin-induced EMT genes, MMP-7 and HB-EGF in carcinogenesis in the INS-GAS mouse stomach was investigated.
The INS-GAS mouse, a transgenic mouse model of gastric carcinogenesis which overexpresses amidated gastrin, was used to investigate the in vivo relationship between HB-EGF, MMP-7, gastrin and EMT.
25 An INS-GAS mouse develops gastric metaplasia, dysplasia, carcinoma and gastric cancer with vascular invasion at 20 months of age; this model shows a direct link between gastrin and gastric cancer.
When his staff gassed mice with hydrogen sulfide at a fraction of the lethal dose for humans, their body temperatures plunged, all movement stopped, and their breathing slowed to just a few breaths per minute.
Insulin-gastrin (INS-GAS) mice are transgenic mice overexpressing amidated gastrin in pancreatic islets that leads to accelerated gastric carcinogenesis.
Both INS-GAS mice that overexpress human amidated gastrin and mice rendered hypergastrinaemic by infusion of gastrin also have perturbed expression of bcl-2 family members (7).
INS-GAS mice were treated with the gastrin immunogen G17DT to reduce serum gastrin levels, with controls treated with an inactive form of the immunogen DT.
This is in contrast to Cui et al. (7) who reported that increased amounts of apoptosis were associated with gastric carcinogenesis in INS-GAS mice.
The INS-GAS mice used in this study were, however, on the FVB/N genetic background, and males demonstrated a greater susceptibility to H. felis-induced pathology compared with females, showing a sex difference between mouse strains.
