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一种新型的 LL-37@NH2@Fe3O4 抑制白血病 K562 细胞增殖：体外研究。

A novel LL-37@NH2@Fe3O4 inhibits the proliferation of the leukemia K562 cells: in-vitro study.

机构信息

Department of Basic Sciences, Faculty of Sciences, Imam Hossein University, Tehran, Iran.

Department of Molecular-Cell Biology, Faculty of Sciences, Lahijan Branch, Islamic Azad University, Lahijan, Iran.

出版信息

Sci Rep. 2024 Sep 27;14(1):22245. doi: 10.1038/s41598-024-71946-7.

DOI:10.1038/s41598-024-71946-7
PMID:39333586
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11436878/
Abstract

LL-37 can inhibit the growth of K562 cancer cells when it is conjugated with iron oxide nanoparticles. In this study, Fe3O4 nanoparticles were synthesized using the co-precipitation method and then modified with the LL-37 peptide through an NH2 bridge. The accuracy of the synthesis process was confirmed through various analytical tests, including FTIR, XRD, FESEM, and EDX. To assess the treatment's effectiveness, a viability test was carried out on K562 leukemia cells and normal peripheral blood mononuclear cells. In addition, flow cytometry and Hoechst staining were used to investigate the mechanism of action of the drug. The expression levels of the Bcl-2, Bax, and TP53 genes in the treated cells and the control group were measured using qRT-PCR. The results indicated that the size of the nanoparticles ranged between 34 and 40 nm. The NH2@LL-37@Fe3O4 nanoparticles more effectively inhibited the growth of cancer cells in a concentration-dependent manner, as compared to Fe3O4 alone. Further analysis revealed that apoptosis occurred through increased expression of TP53 and Bax genes compared to the Bcl-2 gene. Therefore, induction of apoptosis and inhibition of growth in K562 cells was attributed to the impact of iron oxide magnetic nanoparticles conjugated with the LL-37 peptide through the TP53/Bax/Bcl-2 pathway.

摘要

当 LL-37 与氧化铁纳米颗粒结合时，可以抑制 K562 癌细胞的生长。在这项研究中，使用共沉淀法合成了 Fe3O4 纳米颗粒，然后通过 NH2 桥接与 LL-37 肽进行修饰。通过各种分析测试，包括 FTIR、XRD、FESEM 和 EDX，确认了合成过程的准确性。为了评估治疗效果，对 K562 白血病细胞和正常外周血单核细胞进行了活力测试。此外，还使用流式细胞术和 Hoechst 染色来研究药物的作用机制。使用 qRT-PCR 测量了处理细胞和对照组中 Bcl-2、Bax 和 TP53 基因的表达水平。结果表明，纳米颗粒的尺寸在 34 到 40nm 之间。与单独的 Fe3O4 相比，NH2@LL-37@Fe3O4 纳米颗粒更有效地抑制了癌细胞的生长，呈浓度依赖性。进一步分析表明，与 Bcl-2 基因相比，TP53 和 Bax 基因的表达增加导致了细胞凋亡。因此，铁氧化物磁性纳米颗粒与 LL-37 肽通过 TP53/Bax/Bcl-2 途径的结合诱导了 K562 细胞的凋亡和生长抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/7efb5b191c86/41598_2024_71946_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/d8eac60e4678/41598_2024_71946_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/a4a03a879990/41598_2024_71946_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/62814d9d99ec/41598_2024_71946_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/6cd488962bab/41598_2024_71946_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/be92485c5dbe/41598_2024_71946_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/96a3e8c72703/41598_2024_71946_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/e8330edaaa25/41598_2024_71946_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/49baa37c4feb/41598_2024_71946_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/62eb3e1c8fa8/41598_2024_71946_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/2bf6fce51f2b/41598_2024_71946_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/f8b61538b0f6/41598_2024_71946_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/7efb5b191c86/41598_2024_71946_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/d8eac60e4678/41598_2024_71946_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/a4a03a879990/41598_2024_71946_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/62814d9d99ec/41598_2024_71946_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/6cd488962bab/41598_2024_71946_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/be92485c5dbe/41598_2024_71946_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/96a3e8c72703/41598_2024_71946_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/e8330edaaa25/41598_2024_71946_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/49baa37c4feb/41598_2024_71946_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/62eb3e1c8fa8/41598_2024_71946_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/2bf6fce51f2b/41598_2024_71946_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/f8b61538b0f6/41598_2024_71946_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/730c/11436878/7efb5b191c86/41598_2024_71946_Fig12_HTML.jpg

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[1]
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Molecules. 2022-7-15

[2]
Inhibition of -Hemolysin Production Using Nanocurcumin Capped Au@ZnO Nanocomposite.

Bioinorg Chem Appl. 2022-5-28

[3]
Genetic Biomarkers in Chronic Myeloid Leukemia: What Have We Learned So Far?

Int J Mol Sci. 2021-11-19

[4]
Enhancing the anticancer efficacy of a LL-37 peptide fragment analog using peptide-linked PLGA conjugate micelles in tumor cells.

Int J Pharm. 2021-9-5

[5]
Pt(II)-Thiocarbohydrazone Complex as Cytotoxic Agent and Apoptosis Inducer in Caov-3 and HT-29 Cells through the P53 and Caspase-8 Pathways.

Pharmaceuticals (Basel). 2021-5-26

[6]
Human cathelicidin antimicrobial peptide suppresses proliferation, migration and invasion of oral carcinoma HSC-3 cells via a novel mechanism involving caspase-3 mediated apoptosis.

Mol Med Rep. 2020-12

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Down-regulation of Survivin and Bcl-2 concomitant with the activation of caspase-3 as a mechanism of apoptotic death in KG1a and K562 cells upon exposure to a derivative from ciprofloxacin family.

Toxicol Appl Pharmacol. 2020-12-15

[8]
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N Engl J Med. 2020-7-30

[9]
Novel pyridinecarboxaldehyde thiosemicarbazone conjugated magnetite nanoparticulates (MNPs) promote apoptosis in human lung cancer A549 cells.

J Biol Inorg Chem. 2020-2

[10]
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