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Immunohistochemical analysis of Omi/HtrA2 expression in stomach cancer
Author(s) -
LEE SUG HYUNG,
LEE JONG WOO,
KIM HONG SUG,
KIM SU YOUNG,
PARK WON SANG,
KIM SANG HO,
LEE JUNG YOUNG,
YOO NAM JIN
Publication year - 2003
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1034/j.1600-0463.2003.1110508.x
Subject(s) - apoptosis , cancer , immunohistochemistry , cancer research , stomach cancer , cancer cell , caspase , biology , programmed cell death , serine protease , stomach , pathology , medicine , protease , biochemistry , enzyme
The serine protease Omi/HtrA2 is released from mitochondria into the cytosol after apoptosis stimuli, inducing apoptosis in a caspase‐independent manner through its protease activity and in a caspase‐dependent manner by neutralizing the inhibition of inhibitor of apoptosis proteins (IAPs) on caspases. Alteration of apoptosis is essential for cancer development, and cancer cell death by radiation and chemotherapy is largely dependent upon apoptosis. Thus, analysis of the expression status of Omi/HtrA2, a regulator of apoptosis, in cancer tissues is needed for an understanding of cancer development. In the current study, we analyzed the expression of Omi/HtrA2 in 60 advanced gastric adenocarcinomas by immunohistochemistry using a tissue microarray approach. Immunopositivity (defined as ≥30%) was observed for Omi/HtrA2 in 43 (72%) of the 60 cancers. By contrast, the surface mucous cells and mucous neck cells in the normal gastric mucosa showed no or weak expression of Omi/HtrA2. Taken together, these results suggest that stomach cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in stomach cancer development.