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富含半胱氨酸和甘氨酸的蛋白2：一种通过激活JAK-STAT1通路抑制胶质瘤细胞坏死性凋亡的重要调节因子。

Cysteine‑ and glycine‑rich protein 2: A vital regulator that inhibits necroptosis glioma cell by activating the JAK‑STAT1 pathways.

作者信息

Lv Dongsheng, Han Xu, Hao Liang, Sun Zhimin, Zhang Aobo, Liu Jing, Liu Liang, Liu Liqiang

机构信息

Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, P.R. China.

Department of Neurology, The Second Hospital of Shijiazhuang, Shijiazhuang, Hebei 050051, P.R. China.

出版信息

Oncol Rep. 2025 Mar;53(3). doi: 10.3892/or.2025.8873. Epub 2025 Feb 7.

DOI:10.3892/or.2025.8873
PMID:39918019
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11826106/
Abstract

Cysteine‑ and glycine‑rich protein 2 (CSRP2) are closely associated with tumor invasion and metastasis. CSRP2 is significantly upregulated in glioma tissues and is associated with the clinical stage of the tumor. Overexpression of CSRP2 in glioma cells promotes the proliferation and metastasis of cancer cells, whereas CSRP2 knockdown inhibits the biological functions of tumor cells. Transcriptome sequencing of CSRP2‑knockdown U251M cells revealed that silencing of CSRP2 inhibited the JAK‑STAT1 signaling pathway, and differentially expressed genes were significantly enriched in cell processes related to necroptosis. Experiments on necroptosis in glioma cells using flow cytometry, Hoechst 33342/PI dual staining and transmission electron microscopy indicated that CSRP2 overexpression inhibited necroptosis in glioma cells. Western blotting results showed that overexpression of CSRP2 activated the JAK‑STAT1 signaling pathway, while the addition of the pathway inhibitor ruxolitinib promoted the phosphorylation of necroptosis proteins RIPK1, RIPK3 and MLKL. Therefore, it was hypothesized that CSRP2 maintains JAK‑STAT1 activation by inhibiting the protein inhibitor of activated STAT1, which then inhibits the necrotizing apoptosis of glioma cells.

摘要

富含半胱氨酸和甘氨酸的蛋白2（CSRP2）与肿瘤侵袭和转移密切相关。CSRP2在胶质瘤组织中显著上调，且与肿瘤的临床分期相关。CSRP2在胶质瘤细胞中的过表达促进癌细胞的增殖和转移，而敲低CSRP2则抑制肿瘤细胞的生物学功能。对敲低CSRP2的U251M细胞进行转录组测序发现，CSRP2的沉默抑制了JAK-STAT1信号通路，差异表达基因在与坏死性凋亡相关的细胞过程中显著富集。使用流式细胞术、Hoechst 33342/PI双染和透射电子显微镜对胶质瘤细胞进行坏死性凋亡实验表明，CSRP2过表达抑制胶质瘤细胞的坏死性凋亡。蛋白质印迹结果显示，CSRP2的过表达激活了JAK-STAT1信号通路，而添加该通路抑制剂鲁索替尼则促进了坏死性凋亡蛋白RIPK1、RIPK3和MLKL的磷酸化。因此，推测CSRP2通过抑制活化STAT1的蛋白抑制剂来维持JAK-STAT1的激活，进而抑制胶质瘤细胞的坏死性凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/d23c9e2153fc/or-53-03-08873-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/48335de08624/or-53-03-08873-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/e81a7fcd6b69/or-53-03-08873-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/73ac56f9464b/or-53-03-08873-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/3bc227df2288/or-53-03-08873-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/6ab2cf4a512d/or-53-03-08873-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/b450fc910ade/or-53-03-08873-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/ea868261bcbf/or-53-03-08873-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/b563276e6ef5/or-53-03-08873-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/d23c9e2153fc/or-53-03-08873-g08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/48335de08624/or-53-03-08873-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/e81a7fcd6b69/or-53-03-08873-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/73ac56f9464b/or-53-03-08873-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/3bc227df2288/or-53-03-08873-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/6ab2cf4a512d/or-53-03-08873-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/b450fc910ade/or-53-03-08873-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/ea868261bcbf/or-53-03-08873-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/b563276e6ef5/or-53-03-08873-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f48/11826106/d23c9e2153fc/or-53-03-08873-g08.jpg

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