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The progression of HMGB1-induced autophagy in cancer biology

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


Tianwei Xu,* Lihua Jiang,* Zhaoxia Wang

Department of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China

*
These authors contributed equally to this work

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

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