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SFXN3 是一个预后标志物，并促进急性髓系白血病的生长。

SFXN3 is a Prognostic Marker and Promotes the Growth of Acute Myeloid Leukemia.

机构信息

Department of Hematology, the First Affiliated Hospital of Anhui Medical University, Hefei, 230000, China.

Anhui Public Health Clinical Center, Hefei, China.

出版信息

Cell Biochem Biophys. 2024 Sep;82(3):2195-2204. doi: 10.1007/s12013-024-01326-5. Epub 2024 Jun 14.

DOI:10.1007/s12013-024-01326-5
PMID:38877336
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11445304/
Abstract

Acute myeloid leukemia (AML) is a heterogeneous disease with rapid progression and frequent mutations. Sideroflexin3 (SFXN3) has been shown to be involved in various neurodegenerative diseases. However, the role of SFXN3 in AML remains unclear. The level and prognostic value of SFXN3 were assessed in pan-cancer, especially AML, based on the data obtained from the TCGA database. The effect and mechanism of SFXN3 in AML were measured by fluorescence-activated cell sorting (FACS), qRT-PCR, western blotting in vitro and in vivo. The correlation between SFXN3 and the infiltration of immune cells in AML was assessed via cibersort and ssGSEA analyses. SFXN3 is expressed at higher levels in AML, and high SFXN3 level is associated with decreased overall survival rate (OSR) in AML. Next, knockdown of SFXN3 results in enhanced cell apoptosis and dropped cell proliferation. Then, knockdown of SFXN3 caused a reduction in the expression of CyclinD1 (CCND1) and nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (NFKB1). Finally, SFXN3 may related to the immunosuppressive state of AML. Increased SFXN3 expression is detected in AML, which indicates a poor prognosis and may link to immunosuppressive state of AML. In addition, SFXN3 can inhibit AML cells apoptosis and promote cell proliferation via enhancing CCND1 and NFKB1 levels.

摘要

急性髓系白血病（AML）是一种进展迅速、频繁发生突变的异质性疾病。Sideroflexin3（SFXN3）已被证明参与多种神经退行性疾病。然而，SFXN3 在 AML 中的作用尚不清楚。基于 TCGA 数据库获得的数据，评估了 SFXN3 在泛癌中的水平和预后价值，特别是在 AML 中。通过体外和体内荧光激活细胞分选（FACS）、qRT-PCR、western blot 测定了 SFXN3 在 AML 中的作用及其机制。通过 cibersort 和 ssGSEA 分析评估了 SFXN3 与 AML 中免疫细胞浸润的相关性。SFXN3 在 AML 中表达水平较高，高水平的 SFXN3 与 AML 患者总生存率（OSR）降低相关。接下来，敲低 SFXN3 导致细胞凋亡增强和增殖下降。然后，敲低 SFXN3 导致细胞周期蛋白 D1（CCND1）和 B 细胞κ轻肽基因增强子核因子 1（NFKB1）的表达减少。最后，SFXN3 可能与 AML 的免疫抑制状态有关。在 AML 中检测到 SFXN3 表达增加，表明预后不良，可能与 AML 的免疫抑制状态有关。此外，SFXN3 通过增强 CCND1 和 NFKB1 水平抑制 AML 细胞凋亡并促进细胞增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/968c7f387810/12013_2024_1326_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/b29f896f5066/12013_2024_1326_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/077b6773a080/12013_2024_1326_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/4b5a6cdd15b1/12013_2024_1326_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/9d47115b7b69/12013_2024_1326_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/f52565c98317/12013_2024_1326_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/968c7f387810/12013_2024_1326_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/b29f896f5066/12013_2024_1326_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/077b6773a080/12013_2024_1326_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/4b5a6cdd15b1/12013_2024_1326_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/9d47115b7b69/12013_2024_1326_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/f52565c98317/12013_2024_1326_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/092e/11445304/968c7f387810/12013_2024_1326_Fig6_HTML.jpg

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