Abstract:
: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, МСР-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.
journal_name
Mediators Inflammjournal_title
Mediators of inflammationauthors
Makeeva A,Rodriguez-Montesinos J,Zelenikhin P,Nesmelov A,Preissner KT,Cabrera-Fuentes HA,Ilinskaya ONdoi
10.1155/2017/4029641subject
Has Abstractpub_date
2017-01-01 00:00:00pages
4029641eissn
0962-9351issn
1466-1861journal_volume
2017pub_type
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