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The progression of HMGB1-induced autophagy in cancer biology
Tianwei Xu1, Lihua Jiang1, Zhaoxia Wang1
1Department of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China, wangzhaoxia@njmu.edu.cn.
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.
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