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长链非编码RNA CRNDE通过调控PI3K/AKT/mTOR信号通路促进舌鳞状细胞癌的进展。

Long non-coding RNA CRNDE promote the progression of tongue squamous cell carcinoma through regulating the PI3K/AKT/mTOR signaling pathway.

作者信息

Yang Zhongheng, Chen Weizhi

机构信息

Department of Stomatology, The First Affiliated Hospital of Jinzhou Medical University Jinzhou China.

Department of Radiology, The First Affiliated Hospital of Jinzhou Medical University No. 2, Renmin Rd, Guta District 121001 Jinzhou Liaoning China

出版信息

RSC Adv. 2019 Jul 10;9(37):21381-21390. doi: 10.1039/c9ra01321k. eCollection 2019 Jul 5.

DOI:10.1039/c9ra01321k
PMID:35521355
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9066183/
Abstract

Long non-coding RNAs (lnRNAs) colorectal neoplasia differentially expressed (CRNDE) has been identified as a crucial regulator involved in tongue squamous cell carcinoma (TSCC). However, the molecular mechanism of CRNDE involved in TSCC progression is still unknown. In the study, qRT-PCR assay was used to detect the expression of CRNDE in TSCC tissues and cells. CCK-8 assay, colony formation assay, transwell assay and flow cytometric analysis were performed to determine cell proliferation ability, colony formation, migration and invasion capacities, and cell apoptosis, respectively. Western blot was employed to assess the activity of the PI3K/AKT/mTOR pathway. A xenograft mice model was performed to evaluate the role of CRNDE on tumor growth . The results showed CRNDE was upregulated in TSCC tissues and cell lines. CRNDE knockdown repressed the proliferation, colony formation, migration and invasion and promoted apoptosis in TSCC cells. Moreover, CRNDE regulated the PI3K/AKT/mTOR pathway in TSCC cells. Additionally, high levels of CRNDE inhibited tumor growth . In conclusion, high levels of CRNDE might promote TSCC progression at least partly through regulating the PI3K/AKT/mTOR pathway. Targeting CRNDE has potential to be used as a novel target of TSCC treatment.

摘要

长链非编码RNA(lnRNA)结直肠癌差异表达基因(CRNDE)已被确定为参与舌鳞状细胞癌(TSCC)的关键调节因子。然而,CRNDE参与TSCC进展的分子机制仍不清楚。在本研究中,采用qRT-PCR检测TSCC组织和细胞中CRNDE的表达。分别进行CCK-8检测、集落形成检测、Transwell检测和流式细胞术分析,以确定细胞增殖能力、集落形成、迁移和侵袭能力以及细胞凋亡情况。采用蛋白质免疫印迹法评估PI3K/AKT/mTOR信号通路的活性。建立异种移植小鼠模型以评估CRNDE对肿瘤生长的作用。结果显示,CRNDE在TSCC组织和细胞系中上调。敲低CRNDE可抑制TSCC细胞的增殖、集落形成、迁移和侵袭,并促进其凋亡。此外,CRNDE在TSCC细胞中调节PI3K/AKT/mTOR信号通路。另外,高水平的CRNDE抑制肿瘤生长。综上所述,高水平的CRNDE可能至少部分通过调节PI3K/AKT/mTOR信号通路促进TSCC进展。靶向CRNDE有潜力作为TSCC治疗的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6ab/9066183/f5ae7f0bad79/c9ra01321k-f6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6ab/9066183/f5ae7f0bad79/c9ra01321k-f6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6ab/9066183/4f3202d32537/c9ra01321k-f2.jpg
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