论文已发表
注册即可获取德孚的最新动态
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Authors Xu T, Jiang L, Wang Z
Received 30 August 2018
Accepted for publication 18 November 2018
Published 31 December 2018 Volume 2019:12 Pages 365—377
DOI https://doi.org/10.2147/OTT.S185876
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Geoffrey Pietersz
Abstract: Autophagy is an important process of cellular degradation and
has been proven to contribute to tumorigenesis. High-mobility group box 1
(HMGB1) is an abundant nonhistone protein that has been widely reported to play
a central role in the induction of autophagy. In nucleus, HMGB1 upregulates the
expression of HSP27 to induce autophagy. In cytoplasm, the Beclin-1/PI3K-III
complex can be activated by HMGB1 to promote autophagy. Extracellular HMGB1
binds to the receptor for advanced glycation end products to induce autophagy.
Recent studies have shown that HMGB1-induced autophagy exerts multiple
functions in various cancers like proliferation. Moreover, inhibition of
HMGB1-induced autophagy can reverse chemoresistance, which is regulated by
noncoding RNAs such as microRNAs and lncRNAs. Here, we provide a brief
introduction to HMGB1 and HMGB1-induced autophagy in cancer. We also discuss
the challenges associated with performing further investigations on this issue.
HMGB1-induced autophagy exerts significant functions in cancer and has
potential utility for new strategy to reverse drug resistance.
Keywords: HMGB1,
autophagy, cancer, noncoding RNA, drug resistance