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二硫化二砷促进弥漫性大 B 细胞淋巴瘤细胞中 的去甲基化。

Arsenic disulfide promoted the demethylation of in diffuse large B cell lymphoma cells.

机构信息

Department of Hematology, The Affiliated Taian City Central Hospital of Qingdao University, Taian, Shandong, China.

Department of Breast Surgery, The Affiliated Taian City Central Hospital of Qingdao University, Taian, Shandong, China.

出版信息

PeerJ. 2024 May 14;12:e17363. doi: 10.7717/peerj.17363. eCollection 2024.

DOI:10.7717/peerj.17363
PMID:38766487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11100478/
Abstract

BACKGROUND

Promoter hypermethylation of the tumor suppressor gene is one of the well-studied causes of cancer development. The drugs that reverse the process by driving demethylation could be a candidate for anticancer therapy. This study was designed to investigate the effects of arsenic disulfide on methylation in diffuse large B cell lymphoma (DLBCL).

METHODS

We knocked down the expression of in two DLBCL cell lines (, DB and SU-DHL-4 cells) using siRNA. Then the DLBCL proliferation was determined in the presence of knockdown. The methylation of in DLBCL cells was analyzed by methylation specific PCR (MSPCR). The effect of arsenic disulfide on the methylation was determined in DLBCL cell lines in the presence of different concentrations of arsenic disulfide (5 µM, 10 µM and 20 µM), respectively. To investigate the potential mechanism on the arsenic disulfide-mediated methylation, the mRNA expression of , and was determined.

RESULTS

functioned as a tumor suppressor gene in DLBCL cells, which was featured by the fact that knockdown promoted the proliferation of DLBCL cells. was found hypermethylated in DLBCL cells. Arsenic disulfide promoted the demethylation in a dose-dependent manner, which was related to the inhibition of DNMTs and the increase of MBD2.

CONCLUSION

Experimental evidence shows that functions as a tumor suppressor gene in DLBCL progression. hyper-methylation could be reversed by arsenic disulfide in a dose-dependent manner.

摘要

背景

肿瘤抑制基因启动子的异常高甲基化是癌症发展的一个重要研究方向。能够逆转这一过程的去甲基化药物可能成为抗癌治疗的候选药物。本研究旨在探讨二硫化二砷对弥漫性大 B 细胞淋巴瘤（DLBCL）中甲基化的影响。

方法

我们使用 siRNA 敲低了两种 DLBCL 细胞系（和 DB 和 SU-DHL-4 细胞）中的表达。然后在的敲低存在下测定 DLBCL 增殖。通过甲基化特异性 PCR（MSPCR）分析 DLBCL 细胞中的甲基化。在不同浓度的二硫化二砷（5 µM、10 µM 和 20 µM）存在下，分别确定二硫化二砷对 DLBCL 细胞系中甲基化的影响。为了研究二硫化二砷介导的甲基化的潜在机制，测定了、和的 mRNA 表达。

结果

在 DLBCL 细胞中，作为肿瘤抑制基因，其特征是敲低促进了 DLBCL 细胞的增殖。发现在 DLBCL 细胞中呈高甲基化状态。二硫化二砷以剂量依赖性方式促进甲基化，这与 DNMTs 的抑制和 MBD2 的增加有关。

结论

实验证据表明在 DLBCL 进展中作为肿瘤抑制基因发挥作用。二硫化二砷可以剂量依赖性方式逆转异常高甲基化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/07726483677e/peerj-12-17363-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/85662cbd129d/peerj-12-17363-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/f57d5e0cd410/peerj-12-17363-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/427c5a39abfd/peerj-12-17363-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/8b865e410ff9/peerj-12-17363-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/7a22a783a157/peerj-12-17363-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/07726483677e/peerj-12-17363-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/85662cbd129d/peerj-12-17363-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/f57d5e0cd410/peerj-12-17363-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/427c5a39abfd/peerj-12-17363-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/8b865e410ff9/peerj-12-17363-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/7a22a783a157/peerj-12-17363-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e39/11100478/07726483677e/peerj-12-17363-g006.jpg

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本文引用的文献

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The Role of DNA Methylation and DNA Methyltransferases in Cancer.DNA甲基化与DNA甲基转移酶在癌症中的作用
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Protein tyrosine phosphatase PTPL1 suppresses lung cancer through Src/ERK/YAP1 signaling.蛋白酪氨酸磷酸酶 PTPL1 通过Src/ERK/YAP1 信号通路抑制肺癌。
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