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自噬在急性髓系白血病治疗中的作用。

Role of autophagy in acute myeloid leukemia therapy.

作者信息

Zhang Su-Ping, Niu Yu-Na, Yuan Na, Zhang Ai-Hong, Chao Dan, Xu Qiu-Ping, Wang Li-Jun, Zhang Xue-Guang, Zhao Wen-Li, Zhao Yun, Wang Jian-Rong

机构信息

Soochow University, Suzhou, Jiangsu, People's Republic of China.

出版信息

Chin J Cancer. 2013 Mar;32(3):130-5. doi: 10.5732/cjc.012.10073. Epub 2012 Aug 2.

DOI:10.5732/cjc.012.10073
PMID:22854065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3845596/
Abstract

Despite its dual role in determining cell fate in a wide array of solid cancer cell lines, autophagy has been robustly shown to suppress or kill acute myeloid leukemia cells via degradation of the oncogenic fusion protein that drives leukemogenesis. However, autophagy also induces the demise of acute leukemia cells that do not express the known fusion protein, though the molecular mechanism remains elusive. Nevertheless, since it can induce cooperation with apoptosis and differentiation in response to autophagic signals, autophagy can be manipulated for a better therapy on acute myeloid leukemia.

摘要

尽管自噬在多种实体癌细胞系中决定细胞命运方面具有双重作用,但已有充分证据表明,自噬可通过降解驱动白血病发生的致癌融合蛋白来抑制或杀死急性髓系白血病细胞。然而,自噬也会诱导不表达已知融合蛋白的急性白血病细胞死亡,尽管其分子机制仍不清楚。尽管如此,由于自噬可诱导与凋亡和分化协同以响应自噬信号,因此可以通过调控自噬来更好地治疗急性髓系白血病。

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本文引用的文献

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Autophagy contributes to therapy-induced degradation of the PML/RARA oncoprotein.自噬有助于治疗诱导的 PML/RARA 癌蛋白降解。
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Arsenic trioxide controls the fate of the PML-RARalpha oncoprotein by directly binding PML.三氧化二砷通过直接结合 PML 来控制 PML-RARα 癌蛋白的命运。
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