USP13 通过促进 ATG5 推动急性髓性白血病细胞增殖和自噬

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2024-08-09 DOI:10.1016/j.tice.2024.102494

Yuchu Yuan , Meizhu Xue , Feng Zhou , Lifang Gu

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引用次数: 0

摘要

目的通过研究 USP13 对细胞生长、凋亡和自噬的影响，阐明 USP13 在急性髓性白血病（AML）中的作用，并探索其潜在机制。采用细胞计数试剂盒-8（CCK-8）和 Edu 染色法评估 USP13 对 AML 细胞生长的影响。进行了末端脱氧核苷酸转移酶 dUTP 缺口标记（TUNEL）和免疫染色试验，以检测 USP13 对 AML 细胞凋亡和自噬的影响，并进行了免疫印迹试验，以确定潜在的机制途径。此外，USP13 还能促进 AML 细胞的自噬。结论USP13通过上调ATG5促进AML细胞生长和自噬。

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USP13 promotes acute myeloid leukemia cell proliferation and autophagy by promoting ATG5

Objective

To elucidate the role of USP13 in acute myeloid leukemia (AML) by investigating its effects on cell growth, apoptosis and autophagy, and to explore the underlying mechanisms.

Methods

The expression of USP13 in AML cells was assessed using quantitative PCR (qPCR) and immunoblotting. Cell Counting Kit-8 (CCK-8) and Edu staining were employed to evaluate the impact of USP13 on AML cell growth. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and immunostaining assays were conducted to examine the effects of USP13 on apoptosis and autophagy in AML cells, and immunoblot assays were performed to determine the potential underlying mechanistic pathway.

Results

USP13 expression was significantly elevated in AML cells, correlating with enhanced cell proliferation and resistance to apoptosis. Moreover, USP13 promoted autophagy in AML cells. Mechanistically, USP13 was found to be associated with upregulating ATG5 expression, which promoted AML progression.