Premium
The effects of acetylsalicylic acid on proliferation, apoptosis, and invasion of cyclooxygenase‐2 negative colon cancer cells
Author(s) -
Yu H.G.,
Huang J.A.,
Yang Y.N.,
Huang H.,
Luo H.S.,
Yu J.P.,
Meier J. J.,
Schrader H.,
Bastian A.,
Schmidt W. E.,
Schmitz F.
Publication year - 2002
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2002.01080.x
Subject(s) - apoptosis , carcinoembryonic antigen , cancer research , flow cytometry , colorectal cancer , acridine orange , cell culture , cyclooxygenase , cell growth , cancer cell , cancer , chemistry , biology , medicine , immunology , enzyme , biochemistry , genetics
Summary Background Acetylsalicylic acid (ASA, aspirin), the most common nonsteroidal anti‐inflammatory drug (NSAID), has been shown to have a protective effect against the incidence and mortality of colorectal cancer. However, the mechanism of its anticancer function remains unclear. The aim of this study was to determine the effects of acetylsalicylic acid on proliferation, apoptosis, and invasion in human cyclooxygenase‐2 (COX‐2) negative colorectal cancer cell lines. Materials and Methods After treatment with various concentrations of ASA, cell proliferation was measured in the human colon cancer cell line SW480. Apoptotic cells were identified by transmission electron microscopy, acridine orange staining, and flow cytometry. The invasive potential of SW480 cells was detected using an in vitro invasion assay. The production of carcinoembryonic antigen was measured by microparticle enzyme immunoassay. Expression of Bcl 2 , Bax, CD44v6, and nm23 were evaluated by immunocytochemistry. Results ASA significantly inhibited the proliferation of SW480 cells and stimulated apoptosis. Production of carcinoembryonic antigen and the invasive potential of SW480 cells were also inhibited by ASA. After treatment with ASA, down‐regulation of Bcl 2 and CD44v6 expression and up‐regulation of nm23 expression were observed in SW480 cells. No obvious effect of ASA was found on Bax expression. Conclusion Our findings reveal that ASA inhibits the proliferation and promotes apoptosis in the human colon cancer cell line SW480. Down‐regulation of Bcl 2 expression might represent a potential mechanism by which ASA induces apoptosis in this COX‐2 negative colon cancer cell line. Our results also suggest that ASA decreases the invasive potential of these colon cancer cells. Decreased CEA content and CD44v6 expression and elevated nm23 expression may contribute to the effect of ASA on invasive potential of SW480 colon cancer cells.