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Specific expression of the pancreatic‐secretory‐trypsin‐inhibitor (PSTI) gene in hepatocellular carcinoma
Author(s) -
Ohmachi Yoshitaka,
Murata Atsuo,
Yasuda Tadashi,
Yasuda Takushi,
Monden Morito,
Mori Takesada,
Ogawa Michio,
Matsubara Kenichi
Publication year - 1993
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910550505
Subject(s) - psti , biology , cancer research , pancreatic disease , gene expression , hccs , hepatocellular carcinoma , microbiology and biotechnology , gene , pancreas , endocrinology , plasmid , genetics
Twenty hepatocellular carcinomas (HCC) were analyzed by Northern blotting to test the expression of pancreatic secretory trypsin inhibitor (PSTI). This gene was expressed in all HCCs, but not in other tumors, including mammary, thyroid, pulmonary and ovarian cancers. Some gastric and colonic cancers weakly expressed PSTI. Among cell lines examined in a similar manner, PSTI was expressed in all of 4 derived from hepatoma. On the other hand, among 15 cell lines derived from cancers other than hepatoma, only 3, derived from pancreatic, colonic and gastric cancers, weakly expressed PSTI. A CAT assay using a deletion set of the 5′ region from the cloned PSTI gene has shown that in hepatoma cell lines, the expression of this gene is dependent on the presence of 2 regulatory regions that include an IL‐6 responsive element and an AP‐1‐binding site. However, in non‐hepatoma cell lines, the 2 regulatory regions are not necessary for expression. The blood level of PSTI in 27 patients with HCC was significantly increased, and it was positively correlated with tumor size, suggesting that specific expression of PSTI in HCC causes this effect and that elevated blood level of PSTI without inflammation indicates the presence of HCC.