2011
DOI: 10.1007/s00232-010-9309-7
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TNF-α Induced Apoptosis is Accompanied with Rapid CD30 and Slower CD45 Shedding from K-562 Cells

Abstract: TNF-α can induce cell death (apoptosis and necrosis), and these effects mostly depend on expression of TNF-receptor superfamily molecules. As determination of certain intracellular enzymes like LDH, released from cultured tumor cells, reflects early membrane alterations, we compared LDH release with changes in cell surface membrane molecule expression during culture of K-562 cells in the presence of TNF-α. TNF-α-mediated CD45 and CD30 shedding is shown to be to be time- and dose-dependent and associated with s… Show more

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Cited by 113 publications
(46 citation statements)
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“…3A), and (c) several known reagents that inhibit the Tf-TfR intracellular endocytic processing events (e.g., incubation at 16 °C, or in the presence of ammonium chloride, chloroquine, or nocodazole) resulted in a drastic inhibition in the conversion of ProINS-Tf to irINS-Tf (Fig 3B, C, and D). In addition, results of LDH release assay, which is an indicator of membrane integrity [22, 23], suggested that ProINS-Tf fusion proteins did not cause cell membrane destruction to release non-specific cytosolic proteases to the cell surface.…”
Section: Discussionmentioning
confidence: 99%
“…3A), and (c) several known reagents that inhibit the Tf-TfR intracellular endocytic processing events (e.g., incubation at 16 °C, or in the presence of ammonium chloride, chloroquine, or nocodazole) resulted in a drastic inhibition in the conversion of ProINS-Tf to irINS-Tf (Fig 3B, C, and D). In addition, results of LDH release assay, which is an indicator of membrane integrity [22, 23], suggested that ProINS-Tf fusion proteins did not cause cell membrane destruction to release non-specific cytosolic proteases to the cell surface.…”
Section: Discussionmentioning
confidence: 99%
“…There are rare data regarding these NK cell effector functions in patients with MM and it has been shown that lenalidomide, an immunomodulatory agent used in the therapy of this disease, enhances the NK cell arm of the immune response 32. As found in other advanced malignancies, NK cell dysfunction in patients with MM is probably the consequence of cytokine disbalance due to the prevalence of immunosuppressive cytokines such as IL-10, transforming growth factor β (TGFβ) and also IL-6, as well as other tumour-produced inhibitory factors 33 34. These cytokines are involved in tumour-derived immune dysfunction by upregulation of immunosuppressive T regulatory cells, myeloid-derived suppressor cells and enzymes that through different mechanisms, including downregulation of cytotoxic molecules, perforin and granzymes, inhibit NK cell-mediated tumour cytotoxicity 12…”
Section: Discussionmentioning
confidence: 99%
“…Drug resistance is the main cause of therapy failure. It is a multifactor phenomenon which includes different mechanisms leading to evasion of apoptosis [14]. One of the proteins involved in this process is GRP78.…”
Section: Discussionmentioning
confidence: 99%