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SOX9 激活的 PXN-AS1 通过 EZH2 介导的 DKK1 甲基化促进胶质母细胞瘤的发生。

SOX9-activated PXN-AS1 promotes the tumorigenesis of glioblastoma by EZH2-mediated methylation of DKK1.

机构信息

Department of Neurosurgery, School of Medicine, Renji Hospital, Jiaotong University, Shanghai, China.

Department of Pediatric Neurosurgery, Xin Hua Hospital affiliated to School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

出版信息

J Cell Mol Med. 2020 Jun;24(11):6070-6082. doi: 10.1111/jcmm.15189. Epub 2020 Apr 23.

DOI:10.1111/jcmm.15189
PMID:32329150
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7294137/
Abstract

Increasing evidence has validated the essential regulation of long non-coding RNAs (lncRNAs) in the biological process of tumours. LncRNA PXN-AS1 has been discovered to be as a tumour suppressor in pancreatic cancer; however, its function and mechanism remain greatly unknown in glioblastoma (GBM). Our present study indicated that PXN-AS1 was highly expressed in GBM tissues and cells. Besides, the knock-down of PXN-AS1 was closely associated with the inhibitory proliferation and inducing apoptosis of GBM cells. PXN-AS1 inhibition was also found to restrain GBM tumour growth. Importantly, SOX9 functioned as a transcription factor and activated PXN-AS1 expression, and overexpressed PXN-AS1 rescued the inhibitory role of down-regulated SOX9 in GBM cell growth. Subsequently, it was discovered that PXN-AS1 activated Wnt/β-catenin pathway. DKK1 was widely known as an inhibitor gene of Wnt/β-catenin pathway, and its expression was negatively associated with PXN-AS1 and SOX9. Interestingly, we found that PXN-AS1 could recruit EZH2 to mediate the H3K27me3 level of DKK1 promoter. Restoration experiments manifested that DKK1 knock-down counteracted PXN-AS1 depletion-mediated repression in GBM cell growth. All facts pointed out that PXN-AS1 might be of importance in exploring the therapeutic strategies of GBM.

摘要

越来越多的证据证实了长非编码 RNA（lncRNA）在肿瘤生物学过程中的重要调控作用。已经发现 lncRNA PXN-AS1 在胰腺癌中作为一种肿瘤抑制因子；然而，其在胶质母细胞瘤（GBM）中的功能和机制仍知之甚少。我们的研究表明，PXN-AS1 在 GBM 组织和细胞中高表达。此外，敲低 PXN-AS1 与抑制 GBM 细胞增殖和诱导细胞凋亡密切相关。还发现 PXN-AS1 抑制可抑制 GBM 肿瘤生长。重要的是，SOX9 作为转录因子发挥作用并激活 PXN-AS1 的表达，而过表达 PXN-AS1 挽救了下调的 SOX9 在 GBM 细胞生长中的抑制作用。随后，发现 PXN-AS1 激活了 Wnt/β-catenin 通路。DKK1 是 Wnt/β-catenin 通路的抑制剂基因，其表达与 PXN-AS1 和 SOX9 呈负相关。有趣的是，我们发现 PXN-AS1 可以招募 EZH2 来介导 DKK1 启动子的 H3K27me3 水平。恢复实验表明，DKK1 敲低可拮抗 PXN-AS1 耗竭介导的 GBM 细胞生长抑制。所有事实都表明，PXN-AS1 在探索 GBM 的治疗策略方面可能具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/6bd8e29f5e5a/JCMM-24-6070-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/16fb80de008c/JCMM-24-6070-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/0d9532172711/JCMM-24-6070-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/d1b9381a7b36/JCMM-24-6070-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/685d2be141fd/JCMM-24-6070-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/728f7fbc6367/JCMM-24-6070-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/6bd8e29f5e5a/JCMM-24-6070-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/16fb80de008c/JCMM-24-6070-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/0d9532172711/JCMM-24-6070-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/d1b9381a7b36/JCMM-24-6070-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/685d2be141fd/JCMM-24-6070-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/728f7fbc6367/JCMM-24-6070-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4da9/7294137/6bd8e29f5e5a/JCMM-24-6070-g006.jpg

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