当前位置： SCI文献检索 > EXPERIMENTAL CELL RESEARCH期刊下所有文献 > The synthetic tubulysin derivative, tubugi-1, improves the innate immune response by macrophage polarization in addition to its direct cytotoxic effects in a murine melanoma model.

The synthetic tubulysin derivative, tubugi-1, improves the innate immune response by macrophage polarization in addition to its direct cytotoxic effects in a murine melanoma model.

Abstract：

:Synthetic tubugis are equally potent but more stable than their natural forms. Their anticancer potential was estimated on a solid melanoma in vitro and in vivo. Tubugi-1 induced the apoptosis in B16 cells accompanied with strong intracellular production of reactive species, subsequently imposing glutathione and thiol group depletion. Paradoxically, membrane lipids were excluded from the cascade of intracellular oxidation, according to malondialdehyde decrease. Although morphologically apoptosis was typical, externalization of phosphatidylserine (PS) as an early apoptotic event was not detected. Even their exposition is pivotal for apoptotic cell eradication, primary macrophages successfully eliminated PS-deficient tubugi-1 induced apoptotic cells. The tumor volume in animals exposed to the drug in therapeutic mode was reduced in comparison to control as well as to paclitaxel-treated animals. Importantly, macrophages isolated from tubugi-1 treated animals possessed conserved phagocytic activity and were functionally and phenotypically recognized as M1. The cytotoxic effect of tubugi-1 is accomplished through its ability to polarize the macrophages toward M1, probably by PS independent apoptotic cell engulfment. The unique potential of tubugi-1 to prime the innate immune response through the induction of a specific pattern of tumor cell apoptosis can be of extraordinary importance from fundamental and applicable aspects.

journal_name

Exp Cell Res

journal_title

Experimental cell research

authors

Drača D,Mijatović S,Krajnović T,Pristov JB,Đukić T,Kaluđerović GN,Wessjohann LA,Maksimović-Ivanić D

doi

10.1016/j.yexcr.2019.04.028

subject

Has Abstract

pub_date

2019-07-15 00:00:00

pages

159-170

issue

2

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(19)30212-5

journal_volume

380

pub_type

杂志文章

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