Expression of the 100-kda glucose-regulated protein (GRP100/endoplasmin) is associated with tumorigenicity in a model of rat colon adenocarcinoma.

Resistance to glucose starvation and expression of glucose-regulated proteins (grp) were studied in a model of rat colon carcinoma. In this model, various clones originating from the same parental tumor showed distinct tumorigenic potential in syngeneic hosts. Some clones were tumorigenic while others were rejected by an immune-based mechanism. It appeared that the more tumorigenic clones were more resistant to glucose starvation and able to synthesize larger amounts of grp100 than non-tumorigenic clones in response to either glucose starvation or tunicamycin treatment. In contrast, there was no difference in the induced levels of synthesis of grp78 between tumorigenic and non-tumorigenic clones. These results suggest that the ability of cells to synthesize large amounts of the stress protein grp100 might allow them to resist marginal conditions imposed by fully immunocompetent hosts, thus conferring greater tumorigenicity.