OVEREXPRESSION OF MESSENGER-RNA FOR CHOLECYSTOKININ-A RECEPTOR AND NOVEL EXPRESSION OF MESSENGER-RNA FOR GASTRIN (CHOLECYSTOKININ-B) RECEPTOR IN AZASERINE-INDUCED RAT PANCREATIC-CARCINOMA
Wg. Zhou et al., OVEREXPRESSION OF MESSENGER-RNA FOR CHOLECYSTOKININ-A RECEPTOR AND NOVEL EXPRESSION OF MESSENGER-RNA FOR GASTRIN (CHOLECYSTOKININ-B) RECEPTOR IN AZASERINE-INDUCED RAT PANCREATIC-CARCINOMA, Carcinogenesis, 14(10), 1993, pp. 2189-2192
Using receptor binding assays, we have previously demonstrated the ove
rexpression of the high-affinity cholecystokinin (CCK) receptor and th
e novel expression of the gastrin (CCK-B) receptor in the azaserine-in
duced rat pancreatic carcinoma DSL-6. Since cDNA of both the CCK-A rec
eptor (classical pancreatic CCK receptor) coding region and the CCK-B
receptor coding region have recently been cloned and sequenced, we inv
estigated the expression of messenger RNA of these receptors in DSL-6
pancreatic carcinoma. Our results showed that the P-32-labelled cDNA p
robe of the CCK-A receptor coding region hybridized with an almost-equ
al-to 2.7 kb mRNA from both DSL-6 pancreatic carcinoma and normal rat
pancreas. However, the relative expression of the CCK-A receptor mRNA
in DSL-6 pancreatic carcinoma was approximately 8-fold of that in norm
al rat pancreas. The P-32-labelled cDNA probe of the CCK-B receptor co
ding region hybridized with an almost-equal-to 2.7 kb mRNA from DSL-6
pancreatic carcinoma; no hybridizing mRNA could be identified from nor
mal rat pancreas. In summary, the CCK-A receptor mRNA is overexpressed
approximately 8-fold and the gastrin (CCK-B) receptor mRNA is novelly
expressed in DSL-6 pancreatic carcinoma as compared to normal rat pan
creas. These results further confirm our previous findings based on re
ceptor binding assays. The gene overexpression of the CCK-A receptor a
nd the novel gene expression of the gastrin (CCK-B) receptor may be ge
nerated by alterations in gene regulation during carcinogenesis, and m
ay play an important role in promoting tumor growth.