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

IF 2.5 4区生物学 Q1 ANATOMY & MORPHOLOGY Tissue & cell Pub Date : 2024-12-01 Epub Date: 2024-08-09 DOI:10.1016/j.tice.2024.102494

Yuchu Yuan , Meizhu Xue , Feng Zhou , Lifang Gu

{"title":"USP13 promotes acute myeloid leukemia cell proliferation and autophagy by promoting ATG5","authors":"Yuchu Yuan , Meizhu Xue , Feng Zhou , Lifang Gu","doi":"10.1016/j.tice.2024.102494","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><p>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.</p></div><div><h3>Methods</h3><p>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.</p></div><div><h3>Results</h3><p>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.</p></div><div><h3>Conclusion</h3><p>USP13 promotes AML cell growth and autophagy by upregulating ATG5.</p></div>","PeriodicalId":23201,"journal":{"name":"Tissue & cell","volume":"91 ","pages":"Article 102494"},"PeriodicalIF":2.5000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue & cell","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0040816624001952","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/9 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

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.

Conclusion

USP13 promotes AML cell growth and autophagy by upregulating ATG5.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

USP13 通过促进 ATG5 推动急性髓性白血病细胞增殖和自噬

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。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Tissue & cell 医学-解剖学与形态学

CiteScore

3.90

自引率

0.00%

发文量

234

期刊介绍： Tissue and Cell is devoted to original research on the organization of cells, subcellular and extracellular components at all levels, including the grouping and interrelations of cells in tissues and organs. The journal encourages submission of ultrastructural studies that provide novel insights into structure, function and physiology of cells and tissues, in health and disease. Bioengineering and stem cells studies focused on the description of morphological and/or histological data are also welcomed. Studies investigating the effect of compounds and/or substances on structure of cells and tissues are generally outside the scope of this journal. For consideration, studies should contain a clear rationale on the use of (a) given substance(s), have a compelling morphological and structural focus and present novel incremental findings from previous literature.