Sulindac activates nuclear translocation of AIF, DFF40 and endonuclease G but not induces oligonucleosomal DNA fragmentation in HT-29 cells.

[1]  H. H. Kim,et al.  Lactacystin augments the sulindac-induced apoptosis in HT-29 cells , 2003, Apoptosis.

[2]  Y. Yoo,et al.  Synthetic chenodeoxycholic acid derivative HS-1200-induced apoptosis of p815 mastocytoma cells is augmented by co-treatment with lactacystin , 2003, Anti-cancer drugs.

[3]  P. Vandenabeele,et al.  The role of mitochondrial factors in apoptosis: a Russian roulette with more than one bullet , 2002, Cell Death and Differentiation.

[4]  Soo-Jin Jeong,et al.  Genistein-Induced Apoptosis of p815 Mastocytoma Cells Is Mediated by Bax and Augmented by a Proteasome Inhibitor, Lactacystin , 2002, Nutrition and cancer.

[5]  X. Wang.  The expanding role of mitochondria in apoptosis. , 2001, Genes & development.

[6]  Xu Luo,et al.  Endonuclease G is an apoptotic DNase when released from mitochondria , 2001, Nature.

[7]  G. Pons,et al.  Aspirin induces apoptosis through mitochondrial cytochrome c release , 2000, FEBS letters.

[8]  Tak W. Mak,et al.  Two Distinct Pathways Leading to Nuclear Apoptosis , 2000, The Journal of experimental medicine.

[9]  Guido Kroemer,et al.  Mitochondrio‐nuclear translocation of AIF in apoptosis and necrosis , 2000, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[10]  R. Bartrons,et al.  Aspirin induces cell death and caspase-dependent phosphatidylserine externalization in HT-29 human colon adenocarcinoma cells , 1999, British Journal of Cancer.

[11]  S. Korsmeyer,et al.  BCL-2 family members and the mitochondria in apoptosis. , 1999, Genes & development.

[12]  Wengong Wang,et al.  Extracellular matrix inhibits apoptosis and enhances endothelial cell differentiation by a NFκB‐dependent mechanism , 1999, Journal of cellular biochemistry.

[13]  Ruedi Aebersold,et al.  Molecular characterization of mitochondrial apoptosis-inducing factor , 1999, Nature.

[14]  J C Reed,et al.  Mitochondria and apoptosis. , 1998, Science.

[15]  B. Rigas,et al.  Sulindac sulfide induces several subpopulations of colon cancer cells, defined by PCNA/Ki-67 and DNA strand breaks. , 1997, Biochimica et biophysica acta.

[16]  B. Rigas,et al.  Nonsteroidal anti-inflammatory drugs and colorectal cancer: evolving concepts of their chemopreventive actions. , 1997, Gastroenterology.

[17]  Y. Pommier,et al.  7-Hydroxystaurosporine (UCN-01) induces apoptosis in human colon carcinoma and leukemia cells independently of p53. , 1997, Experimental cell research.

[18]  John Calvin Reed.  Double identity for proteins of the Bcl-2 family , 1997, Nature.

[19]  G. Piazza,et al.  Apoptosis primarily accounts for the growth-inhibitory properties of sulindac metabolites and involves a mechanism that is independent of cyclooxygenase inhibition, cell cycle arrest, and p53 induction. , 1997, Cancer research.

[20]  B. Rigas,et al.  Staurosporine inhibits the proliferation, alters the cell cycle distribution and induces apoptosis in HT-29 human colon adenocarcinoma cells. , 1996, Cancer letters.

[21]  D. Hicks,et al.  Differential Growth Inhibition by the Aspirin Metabolite Salicylate in Human Colorectal Tumor Cell Lines: Enhanced Apoptosis in Carcinoma and in Vitro-transformed Adenoma Relative to Adenoma Cell Lines , 1996 .

[22]  B. Dynlacht,et al.  The anti-proliferative effect of sulindac and sulindac sulfide on HT-29 colon cancer cells: alterations in tumor suppressor and cell cycle-regulatory proteins. , 1996, Oncogene.

[23]  B. Rigas,et al.  Nonsteroidal antiinflammatory drugs inhibit the proliferation of colon adenocarcinoma cells: effects on cell cycle and apoptosis. , 1996, Experimental cell research.

[24]  Guido Kroemer,et al.  The biochemistry of programmed cell death , 1995, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[25]  P. Pasricha,et al.  The effects of sulindac on colorectal proliferation and apoptosis in familial adenomatous polyposis. , 1995, Gastroenterology.

[26]  B. Rigas,et al.  Sulindac sulfide, an aspirin-like compound, inhibits proliferation, causes cell cycle quiescence, and induces apoptosis in HT-29 colon adenocarcinoma cells. , 1995, The Journal of clinical investigation.

[27]  Gwyn T. Williams.  Programmed cell death: Apoptosis and oncogenesis , 1991, Cell.

[28]  S. Shapiro,et al.  A hypothesis: nonsteroidal anti-inflammatory drugs reduce the incidence of large-bowel cancer. , 1991, Journal of the National Cancer Institute.

[29]  G. Kroemer,et al.  The mitochondrion in apoptosis: how Pandora's box opens , 2001, Nature Reviews Molecular Cell Biology.

[30]  Jean-Claude Martinou,et al.  Breaking the mitochondrial barrier , 2001, Nature Reviews Molecular Cell Biology.

[31]  B. Rigas,et al.  Effect of aspirin on induction of apoptosis in HT-29 human colon adenocarcinoma cells. , 1998, Biochemical pharmacology.

[32]  N. Thornberry,et al.  Control of apoptosis by proteases. , 1997, Advances in pharmacology.

[33]  Y. Higuchi,et al.  Appearance of 1-2 Mbp giant DNA fragments as an early common response leading to cell death induced by various substances that cause oxidative stress. , 1997, Free radical biology & medicine.

[34]  J. Yuan,et al.  Evolutionary conservation of a genetic pathway of programmed cell death , 1996, Journal of cellular biochemistry.

[35]  D. Robinson,et al.  Protein storage vacuoles form de novo during pea cotyledon development. , 1995, Journal of cell science.

[36]  A. Wyllie,et al.  Cell death: the significance of apoptosis. , 1980, International review of cytology.