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hnRNPA2/B1 通过调节 AKT 和 STAT3 通路对脑胶质瘤 U251 细胞增殖和凋亡的影响。

Effect of hnRNPA2/B1 on the proliferation and apoptosis of glioma U251 cells via the regulation of AKT and STAT3 pathways.

机构信息

Department of Emergency Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou 646100, China.

Department of PICU, Baoan Maternal and Child Health Hospital, Jinan University, Shenzhen 518106, China.

出版信息

Biosci Rep. 2020 Jul 31;40(7). doi: 10.1042/BSR20190318.

DOI:10.1042/BSR20190318
PMID:32463472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7350891/
Abstract

Glioma is the most common malignant tumor in the human central nervous system. Although heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) was previously presumed to be a tumor-promoting gene, the relationship between hnRNPA2/B1 and glioma is unclear. Targeting hnRNPA2/B1 interference in glioma cells can significantly inhibit proliferation and increase apoptosis of human glioma cells in vitro. In a tumor xenograft model, knockdown of hnRNPA2/B1 suppressed tumor growth in glioma cells in vivo. In terms of a mechanism, the knockdown of hnRNPA2/B1 led to inactivation of the AKT and STAT3 signaling pathways, which ultimately reduced the expression of B-cell lymphoma-2 (Bcl-2), CyclinD1 and proliferating cell nuclear antigen (PCNA). Collectively, these data suggest that the inhibition of hnRNPA2/B1 can reduce the growth of gliomas through STAT3 and AKT signaling pathways, and this inhibition is expected to be a therapeutic target for gliomas.

摘要

神经胶瘤是人类中枢神经系统中最常见的恶性肿瘤。尽管异质核核糖核蛋白 A2/B1（hnRNPA2/B1）先前被认为是一种促进肿瘤的基因，但 hnRNPA2/B1 与神经胶瘤之间的关系尚不清楚。靶向神经胶瘤细胞中的 hnRNPA2/B1 干扰可以显著抑制体外人神经胶瘤细胞的增殖并增加其凋亡。在肿瘤异种移植模型中，hnRNPA2/B1 的敲低抑制了体内神经胶瘤细胞的肿瘤生长。就机制而言，hnRNPA2/B1 的敲低导致 AKT 和 STAT3 信号通路失活，最终降低了 B 细胞淋巴瘤-2（Bcl-2）、细胞周期蛋白 D1 和增殖细胞核抗原（PCNA）的表达。总的来说，这些数据表明，抑制 hnRNPA2/B1 可以通过 STAT3 和 AKT 信号通路减少神经胶瘤的生长，这种抑制有望成为神经胶瘤的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/2bf4916ad536/bsr-40-bsr20190318-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/4b57434ae412/bsr-40-bsr20190318-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/1f0fd54844e8/bsr-40-bsr20190318-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/10f12a87bbec/bsr-40-bsr20190318-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/6173628c03a9/bsr-40-bsr20190318-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/24b755cce7f7/bsr-40-bsr20190318-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/2bf4916ad536/bsr-40-bsr20190318-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/4b57434ae412/bsr-40-bsr20190318-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/1f0fd54844e8/bsr-40-bsr20190318-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/10f12a87bbec/bsr-40-bsr20190318-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/6173628c03a9/bsr-40-bsr20190318-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/24b755cce7f7/bsr-40-bsr20190318-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7d9/7350891/2bf4916ad536/bsr-40-bsr20190318-g6.jpg

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