Poly (ADP‑ribosylation) of HMGB1 facilitates its acetylation and promotes HMGB1 translocation‑associated chemotherapy‑induced autophagy in leukaemia cells
- Yunyao Li
- Jianwei Xie
- Xinyu Li
- Jianpei Fang
Affiliations: Guangdong Provincial Key Laboratory of Malignant Tumour Epigenetics and Gene Regulation, Sun Yat‑Sen Memorial Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510120, P.R. China, Department of Paediatrics, Sun Yat‑Sen Memorial Hospital of Sun Yat‑Sen University, Guangzhou, Guangdong 510120, P.R. China
- Published online on: November 19, 2019 https://doi.org/10.3892/ol.2019.11116
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et al. This is an open access article distributed under the
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Acute lymphoblastic leukaemia (ALL) is one of the most common and curable types of cancer in paediatric patients. However, chemotherapeutic resistance is a difficult but common obstacle when treating leukaemia in the clinical setting. Studies have demonstrated that drug resistance is partly attributable to autophagy induced by multiple chemotherapeutic agents. As an evolutionarily conserved non‑histone chromatin‑binding protein, high mobility group box protein 1 (HMGB1) is considered to be an important factor in autophagy, and regulates autophagy at multiple levels via different subcellular localisations. In the present study, it was revealed that chemotherapeutic drugs induced autophagy in leukaemia cells and that translocation of HMGB1 from the nucleus to the cytoplasm is an important molecular event in this process. It was further demonstrated that poly (ADP‑ribosylation) of HMGB1 facilitates its acetylation, thereby inducing HMGB1 translocation and ultimately promoting chemotherapy‑induced autophagy in leukaemic cells. Targeted HMGB1 translocation may overcome chemotherapy‑induced autophagy in leukaemia.