Mechanisms involved in the pro- and anti-apoptotic role of NO in human leukemia

Jp, Kolb

doi:10.1038/sj.leu.2401896

Cited by 129 publications

(78 citation statements)

References 88 publications

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“…22,25,118,119 The p53 protein promotes apoptosis through upregulation of the apoptotic proteins Bax and cyclin-dependent kinase p21, and downregulation of the antiapoptotic protein Bcl-2 ( Figure 2). 85 However, Gotoh et al 24 measured no increase of p53 in NO-mediated apoptosis in RAW 264.7 cells stimulated with LPS/IFN-g. Instead, this group proposed a role for the endoplasmic reticulum stress pathway involving the transcription factors ATF6 and CHOP leading to cytochrome c release (Figure 2).…”

Section: Proapoptotic Mechanismsmentioning

confidence: 99%

“…However, it is known that NO induces a rise in cGMP in neutrophils through activation of sGC. 8,83 Given that the cell permeable analogues of cAMP (db-cAMP) and cGMP (db-cGMP) can delay constitutive neutrophil apoptosis, 10 and that a rise in cGMP has been postulated to at least partially account for NOmediated inhibition of apoptosis in other cell types, 84,85 it is possible that an increase in one or other of these cyclic nucleotides mediates the inhibition of apoptosis in neutrophils exposed to low concentrations of NO. A role for cyclic nucleotide (cGMP or cAMP) signalling has also been proposed in NO-mediated inhibition of both constitutive and Fas-triggered eosinophil apoptosis.…”

Section: Antiapoptotic Mechanismsmentioning

confidence: 99%

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Nitric oxide: a key regulator of myeloid inflammatory cell apoptosis

et al. 2003

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Apoptosis of inflammatory cells is a critical event in the resolution of inflammation, as failure to undergo this form of cell death leads to increased tissue damage and exacerbation of the inflammatory response. Many factors are able to influence the rate of apoptosis in neutrophils, eosinophils, monocytes and macrophages. Among these is the signalling molecule nitric oxide (NO), which possesses both anti-and proapoptotic properties, depending on the concentration and flux of NO, and also the source from which NO is derived. This review summarises the differential effects of NO on inflammatory cell apoptosis and outlines potential mechanisms that have been proposed to explain such actions.

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Section: Proapoptotic Mechanismsmentioning

confidence: 99%

Section: Antiapoptotic Mechanismsmentioning

confidence: 99%

Nitric oxide: a key regulator of myeloid inflammatory cell apoptosis

et al. 2003

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“…Although nitric oxide is effective against microbial invaders and tumor cells, osteopontin was found to inhibit its synthesis (157)(158)(159)(160)(161), and therefore, plays an important role in tumor defenses against the immune system (156, 157). Moreover, nitric oxide has been reported to have tumorpromoting effects, however, its role in malignancy is far from being fully understood (162)(163)(164). Osteopontin production by tumor cells could promote tumor growth and metastasis by protecting them from nitric oxide (156,158).…”

Section: Growth Factor Receptor Pathways and Osteopontinmentioning

confidence: 99%

The Role of Osteopontin in Tumor Progression and Metastasis in Breast Cancer

Rodrigues

Teixeira

Schmitt

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

206

144

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The use of cancer biomarkers to anticipate the outlines of disease has been an emerging issue, especially as cancer treatment has made such positive steps in the last few years. Progress in the development of consistent malignancy markers is imminent because advances in genomics and bioinformatics have allowed the examination of immense amounts of data. Osteopontin is a phosphorylated glycoprotein secreted by activated macrophages, leukocytes, and activated T lymphocytes, and is present in extracellular fluids, at sites of inflammation, and in the extracellular matrix of mineralized tissues. Several physiologic roles have been attributed to osteopontin, i.e., in inflammation and immune function, in mineralized tissues, in vascular tissue, and in kidney. Osteopontin interacts with a variety of cell surface receptors, including several integrins and CD44. Binding of osteopontin to these cell surface receptors stimulates cell adhesion, migration, and specific signaling functions. Overexpression of osteopontin has been found in a variety of cancers, including breast cancer, lung cancer, colorectal cancer, stomach cancer, ovarian cancer, and melanoma. Moreover, osteopontin is present in elevated levels in the blood and plasma of some patients with metastatic cancers. Therefore, suppression of the action of osteopontin may confer significant therapeutic activity, and several strategies for bringing about this suppression have been identified. This review looks at the recent advances in understanding the possible mechanisms by which osteopontin may contribute functionally to malignancy, particularly in breast cancer. Furthermore, the measurement of osteopontin in the blood or tumors of patients with cancer, as a way of providing valuable prognostic information, will be discussed based on emerging clinical data. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1087 -97)

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“…As shown in Figure 5a, b and c, Bcl-2 and Mcl-1 protein expression suffered a significant decrease after CD5 hypercross-linking in B-CLL cells from patient group A (Bcl-2 MFIR 26.9 ± 7.7 control vs 12.5 ± 6.6 in CD5 hypercross-linked, P Ͻ 0.01, Mcl-1 MFIR 27.7 ± 7.4 control vs 11.5 ± 5.4, P Ͻ 0.01), while Bax protein expression was significantly increased (MFIR 14.9 ± 10.3 con- trol vs 29.5 ± 6.5, P Ͻ 0.01). Because a functional inducible nitric oxide synthase displaying anti-apoptotic activity was demonstrated in B-CLL and hairy cell leukemia, [25][26][27] we also examined iNOS expression after CD5 hypercross-linking in eight group A and 11 group B patients, and found a significant decrease of its levels in the B-CLL cells of group A patients (MFIR 10.8 ± 3.4 control vs 5.1 ± 2.0, P Ͻ 0.01), as shown in Figure 5d. Nothing significant happened with the expression of these apoptosis-related proteins in the cells from the 11 group B patients tested.…”

Section: Modulation Of the Apoptosis-related Proteins After Cd5 Hypermentioning

confidence: 99%