dc.contributor.author |
Makeeva A. |
|
dc.contributor.author |
Rodriguez-Montesinos J. |
|
dc.contributor.author |
Zelenikhin P. |
|
dc.contributor.author |
Nesmelov A. |
|
dc.contributor.author |
Preissner K. |
|
dc.contributor.author |
Cabrera-Fuentes H. |
|
dc.contributor.author |
Ilinskaya O. |
|
dc.date.accessioned |
2018-04-05T07:09:27Z |
|
dc.date.available |
2018-04-05T07:09:27Z |
|
dc.date.issued |
2017 |
|
dc.identifier.issn |
0962-9351 |
|
dc.identifier.uri |
http://dspace.kpfu.ru/xmlui/handle/net/129750 |
|
dc.description.abstract |
© Copyright 2017 Anna Makeeva et al. Extracellular bacterial ribonucleases such as binase from Bacillus pumilus possess cytotoxic activity against tumor cells with a potential for clinical application. Moreover, they may induce activation of tumor-derived macrophages either into the M1-phenotype with well-documented functions in the regulation of the antitumor immune response or into M2-macrophages that may stimulate tumor growth, metastasis, and angiogenesis. In this study, binase or endogenous RNase1 (but not RNA or short oligonucleotides) stimulated the expression of activated NF-κB p65 subunit in macrophages. Since no changes in MyD88 and TRIF adaptor protein expression were observed, toll-like receptors may not be involved in RNase-related NF-κB pathway activation. In addition, short exposure (0.5 hr) to binase induced the release of cytokines such as IL-6, MCP-1, or TNF-α (but not IL-4 and IL-10), indicative for the polarization into antitumor M1-macrophages. Thus, we revealed increased expression of activated NF-κB p65 subunit in macrophages upon stimulation by binase and RNase1, but not RNA or short oligonucleotides. |
|
dc.relation.ispartofseries |
Mediators of Inflammation |
|
dc.title |
Antitumor macrophage response to bacillus pumilus ribonuclease (Binase) |
|
dc.type |
Article |
|
dc.relation.ispartofseries-volume |
2017 |
|
dc.collection |
Публикации сотрудников КФУ |
|
dc.source.id |
SCOPUS09629351-2017-2017-SID85036662282 |
|