International Journal of Cell Biology / 2010 / Article / Fig 4

Review Article

The Role of Cyclooxygenase-2 in Cell Proliferation and Cell Death in Human Malignancies

Figure 4

Effects of COX-2 inhibitors on apoptosis. Apoptosis can be mainly mediated by two pathways: the mitochondrial, intrinsic, or stress-induced apoptosis, which is activated in response to damaging stresses and the extrinsic pathway, triggered by the binding of ligands to specific death receptors [51]. COX-2 inhibitors are able to modulate stress-induced apoptosis as well as extrinsic apoptosis in several cell types. In this picture, some examples of these interaction discussed in the text are presented for different cell types: LNCaP, prostate cancer; K562, chronic myeloid leukemia; HT29, colorectal cancer; SK-Hep 1 and HLE, human hepatocarcinoma cells; HepG2, hepatocarcinoma; Be17402, hepatocarcinoma; SMMC-7402, hepatocarcinoma; MG-63, osteosarcoma. Abbreviation: AIF: apoptosis-inducing factor; Bcl-2, B cell lymphoma 2; Bid, Bcl-2 interacting domain; Casp, caspase; Cyt, cytochrome C; DD, death domain; DED, death effector domain; DISC, death-inducing silencing complex; PI3K/PKB, phosphatidyl inositol-3 kinase/protein kinase B; FADD, Fas-associated death domain; GSH, glutathione; PTP, transition permeability pore; TNF, tumor necrosis factor; TRAIL, TNF-related-inducing-apoptosis-ligand.

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