当前位置： SCI文献检索 > ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS期刊下所有文献 > Luteolin enhances TRAIL sensitivity in non-small cell lung cancer cells through increasing DR5 expression and Drp1-mediated mitochondrial fission.

Luteolin enhances TRAIL sensitivity in non-small cell lung cancer cells through increasing DR5 expression and Drp1-mediated mitochondrial fission.

Abstract：

:Cancer cells exhibit extreme sensitivity to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) over normal cells, highlighting TRAIL's potential as a novel and effective cancer drug. However, the therapeutic effect of TRAIL is limited due to drug resistance. In the present study, we sought to investigate the potential effects of luteolin as a TRAIL sensitizer in non-small cell lung cancer (NSCLC) cells. A549 and H1975 cells had low sensitivity or were resistant to TRAIL. Luteolin alone or in combination with TRAIL decreased cell viability and increased apoptosis. Furthermore, luteolin alone or in combination with TRAIL enhanced death receptor 5 (DR5) expression and dynamin-related protein 1 (Drp1)-dependent mitochondrial fission. However, the synergistic effect of luteolin on cell viability and apoptosis was reversed by DR5 and Drp1 inhibition, suggesting that DR5 upregulation and mitochondrial dynamics may be essential for luteolin as a sensitizer of TRAIL-based therapy in NSCLC. Moreover, luteolin treatment alone or in combination with TRAIL increased the phosphorylation of c-Jun N-terminal kinase (JNK), while SP600125 (the JNK inhibitor) significantly abolished the synergistic effect on DR5 expression and Drp1 translocation, indicating that JNK signaling activation was greatly associated with the synergistic effect exerted by luteolin in NSCLC cells. Therefore, TRAIL combined with luteolin could be as an effective chemotherapeutic strategy for NSCLC.

journal_name

Arch Biochem Biophys

journal_title

Archives of biochemistry and biophysics

authors

Wu B,Xiong J,Zhou Y,Wu Y,Song Y,Wang N,Chen L,Zhang J

doi

10.1016/j.abb.2020.108539

subject

Has Abstract

pub_date

2020-10-15 00:00:00

pages

108539

eissn

0003-9861

issn

1096-0384

pii

S0003-9861(20)30548-8

journal_volume

692

pub_type

杂志文章

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