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Mesenchymal stem cells derived from multiple myeloma patients protect against chemotherapy through autophagy-dependent activation of NF-κB signaling.

Abstract：

:Chemotherapy resistance has been considered as a major problem for multiple myeloma (MM) treatment and bone marrow microenvironment plays a crucial role in the MM progression and chemoresistance. Recent studies reported that bone marrow mesenchymal stem cells derived from MM patients (MM-MSCs) revealed various characteristics compared with these from healthy subjects (NM-MSCs). However, the functions and mechanisms by which MM-MSCs mediate the chemotherapy resistance of MM remain unclear. In this study, we show that MM-MSCs decreased melphalan or doxorubicin-induced cell cycle arrest and apoptosis in two MM cell lines (U266 and RPMI-8226). Mechanistically, we demonstrate that MM-MSCs promote the expressions of autophagy related genes to activate autophagy, followed by ultimately NF-κB signaling activation in MM cells. Inhibition of NF-κB signaling reversed the protective effects of MM-MSC on MM cells. Moreover, autophagy inhibitor chloroquine (CQ) or 3-Methyladenine (3MA) treatment significantly suppressed phosphorylation and consequently degradation of NF-κB inhibitor I-κBα, reduced MM-MSCs-mediate activation of NF-κB and prevented MM-MSCs-induced resistance. Taken together, our findings indicate MM-MSCs are involved in the mechanism of the chemotherapy resistance of MM. Therefore, the inhibition of MM-MSCs-induced autophagy may combat chemotherapy resistance and provide a promising therapeutic strategy for MM treatment.

journal_name

Leuk Res

journal_title

Leukemia research

authors

Yang H,Zheng Y,Zhang Y,Cao Z,Jiang Y

doi

10.1016/j.leukres.2017.07.002

subject

Has Abstract

pub_date

2017-09-01 00:00:00

pages

82-88

eissn

0145-2126

issn

1873-5835

pii

S0145-2126(17)30467-8

journal_volume

60

pub_type

杂志文章

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