当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Cytochalasin E increased the sensitivity of human lung cancer A549 cells to bortezomib via inhibition of autophagy.

Cytochalasin E increased the sensitivity of human lung cancer A549 cells to bortezomib via inhibition of autophagy.

Abstract：

:Cancer cells enhance autophagic activity as a survival measure against metabolic and therapeutic stresses. The inhibition of autophagy may represent a valuable sensitizing target for cancer treatment. Recently, we examined the ability of various cytochalasins to inhibit autophagy and demonstrated the potent inhibitory effect of cytochalasin E (CE) on autophagic flux. The present study was conducted to investigate whether CE inhibited autophagosome-lysosome fusion, and to determine whether CE enhanced chemotherapy-induced cell death. Cell exposure to CE led to the accumulation of microtubule-associated protein light chain 3-II (LC3-II) and sequestosome-1/ubiquitin-binding protein p62 (SQSTM1/p62) in a dose- and time-dependent manner. Cells treated with CE exhibited distinct formation of p62-positive structures on lysosome-associated membrane protein 2 (LAMP2)-positive lysosomal vesicles. CE treatment following serum starvation robustly reduced cell viability and increased expression levels of LC3-II and p62, in comparison to those of cells treated with CE alone. Furthermore, combination treatment with CE and bortezomib, an inhibitor of the 26S proteasome, showed a synergistic effect in targeting human lung cancer A549 cells. Altogether, our results demonstrated that CE treatment inhibited autophagosome-lysosome fusion, and this activity, in part, augmented bortezomib-induced cell death. Therefore, we concluded that CE may be a potentially effective therapeutic agent against lung cancer, especially in a combination therapy with proteasome inhibitors.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Takanezawa Y,Nakamura R,Kojima Y,Sone Y,Uraguchi S,Kiyono M

doi

10.1016/j.bbrc.2018.03.029

subject

Has Abstract

pub_date

2018-04-06 00:00:00

pages

603-608

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)30503-5

journal_volume

498

pub_type

杂志文章

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