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Targeting autophagy enhances apatinib-induced apoptosis via endoplasmic reticulum stress for human colorectal cancer.

Abstract：

:Apatinib, a novel tyrosine kinase inhibitor (TKI), has been confirmed for its efficacy and safety in the treatment of advanced gastric carcinoma and some other solid tumors. However, the direct functional mechanisms of tumor lethality mediated by apatinib have not yet been fully characterized, and the precise mechanisms of drug resistance are largely unknown. Here, in this study, we demonstrated that apatinib could induce both apoptosis and autophagy in human colorectal cancer (CRC) via a mechanism that involved endoplasmic reticulum (ER) stress. Moreover, activation of the IRE1α pathway from apatinib-induced ER stress is responsible for the induction of autophagy; however, blocking autophagy could enhance the apoptosis in apatinib-treated human CRC cell lines. Furthermore, the combination of apatinib with autophagy inhibitor chloroquine (CQ) tends to have the most significant anti-tumor effect of CRC both in vitro and in vivo. Overall, our data show that because apatinib treatment could induce ER stress-related apoptosis and protective autophagy in human CRC cell lines, targeting autophagy is a promising therapeutic strategy to relieve apatinib drug resistance in CRC.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Cheng X,Feng H,Wu H,Jin Z,Shen X,Kuang J,Huo Z,Chen X,Gao H,Ye F,Ji X,Jing X,Zhang Y,Zhang T,Qiu W,Zhao R

doi

10.1016/j.canlet.2018.05.046

subject

Has Abstract

pub_date

2018-09-01 00:00:00

pages

105-114

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(18)30385-9

journal_volume

431

pub_type

杂志文章

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