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一种新型长链非编码RNA,RPL34-AS1,通过调节血管内皮生长因子A(VEGFA)促进胶质瘤的增殖和血管生成。

A novel lncRNA, RPL34-AS1, promotes proliferation and angiogenesis in glioma by regulating VEGFA.

作者信息

Zhang Dongzhi, Jiang Haiping, Ye Junyi, Gao Ming, Wang Xinzhuang, Lu Enzhou, Yang He, Wang Lixiang, Zhao Shiguang

机构信息

Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Key Colleges and Universities Laboratory of Neurosurgery in Heilongjiang Province, Harbin, China.

出版信息

J Cancer. 2021 Aug 27;12(20):6189-6197. doi: 10.7150/jca.59337. eCollection 2021.

DOI:10.7150/jca.59337
PMID:34539892
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8425216/
Abstract

Brain gliomas are the most common primary malignant tumors of the central nervous system and one of the leading causes of death in patients with intracranial tumors. The lncRNA RPL34-AS1 is significantly upregulated in glioma tissues. However, the biological function of RPL34-AS1, especially in proliferation in glioma, remains unclear. The role of RPL34-AS1 in proliferation and angiogenesis in glioma cells was investigated using the LN229, U87, and U251 glioma cell lines. The levels of RPL34-AS1 were detected using real-time quantitative reverse transcription polymerase chain reaction. CCK-8 and colony formation assays were performed to determine the role of RPL34-AS1 in proliferation and survival, and its role in angiogenesis was assessed by an endothelial tube formation assay. Changes in protein levels were assessed by western blotting. RPL34-AS1 was upregulated in glioma tissues and was correlated with tumor grade. RPL34-AS1 expression was also higher in glioma cells than in normal astrocytes. Knockdown of RPL34-AS1 blocked glioma cell proliferation by inhibiting angiogenesis. This effect occurred through decreased ERK/AKT signaling. This study suggests that RPL34-AS1 affects cell proliferation and angiogenesis in glioma and therefore may potentially serve as a valuable diagnostic and prognostic biomarker and therapeutic target in patients with glioma.

摘要

脑胶质瘤是中枢神经系统最常见的原发性恶性肿瘤,也是颅内肿瘤患者的主要死亡原因之一。lncRNA RPL34-AS1在胶质瘤组织中显著上调。然而,RPL34-AS1的生物学功能,尤其是在胶质瘤增殖中的功能,仍不清楚。使用LN229、U87和U251胶质瘤细胞系研究了RPL34-AS1在胶质瘤细胞增殖和血管生成中的作用。使用实时定量逆转录聚合酶链反应检测RPL34-AS1的水平。进行CCK-8和集落形成试验以确定RPL34-AS1在增殖和存活中的作用,并通过内皮管形成试验评估其在血管生成中的作用。通过蛋白质印迹评估蛋白质水平的变化。RPL34-AS1在胶质瘤组织中上调,并与肿瘤分级相关。RPL34-AS1在胶质瘤细胞中的表达也高于正常星形胶质细胞。敲低RPL34-AS1可通过抑制血管生成来阻断胶质瘤细胞的增殖。这种作用是通过降低ERK/AKT信号传导发生的。本研究表明,RPL34-AS1影响胶质瘤中的细胞增殖和血管生成,因此可能潜在地作为胶质瘤患者有价值的诊断和预后生物标志物及治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/31fceffcaf56/jcav12p6189g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/760ecbf74018/jcav12p6189g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/4967e5422097/jcav12p6189g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/30d705af9087/jcav12p6189g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/5723ccadee57/jcav12p6189g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/31fceffcaf56/jcav12p6189g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/760ecbf74018/jcav12p6189g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/4967e5422097/jcav12p6189g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/30d705af9087/jcav12p6189g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/5723ccadee57/jcav12p6189g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0762/8425216/31fceffcaf56/jcav12p6189g007.jpg

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