The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma.
The long non-coding RNA AK001796 contributes to tumor growth via regulating expression of p53 in esophageal squamous cell carcinoma.
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DOI：
10.1186/s12935-018-0537-8
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发表时间：
2018
影响因子：
5.8
通讯作者：
Chen YJ
中科院分区：
文献类型：
--
作者：
Liu B;Pan CF;Yao GL;Wei K;Xia Y;Chen YJ
食管鳞状细胞癌（Esophageal squamous cell carcinoma，ESCC）是世界范围内最常见的恶性肿瘤之一。鉴于食管鳞癌预后差，本研究旨在探讨长链非编码RNA（lncRNA）AK 001796对体外细胞增殖、细胞周期及体内致瘤性的影响，为食管鳞癌的治疗提供靶点。采用真实的时间定量PCR方法检测lncRNA AK 001796在食管鳞癌及癌旁组织中的表达水平，并分析其与食管鳞癌患者临床病理特征的相关性。在此基础上，我们敲低了人食管鳞癌细胞系Eca-109和TE-1中lncRNA AK 001796的表达，并利用流式细胞仪检测了这些细胞的细胞周期和凋亡情况。随后，我们用CCK-8法检测lncRNA AK 001796沉默的ESCC细胞的增殖能力，并通过western blot分析这些细胞中的MDM 2/p53信号通路。最后，建立食管鳞癌移植瘤模型，验证lncRNA AK 001796在食管鳞癌发生发展中的作用。在这项研究中，我们证明了与邻近的非肿瘤组织相比，lncRNA AK 001796在ESCC肿瘤组织中显著上调。在异种移植小鼠模型中，lncRNA AK 001796的敲低通过调节MDM 2/p53信号通路抑制ESCC细胞生长、细胞周期和肿瘤生长。lncRNA AK 001796的表达与人ESCC样品中的MDM 2水平正相关。总之，lncRNA AK 001796通过调节ESCC中的MDM 2/p53信号来调节细胞增殖和细胞周期，这为ESCC的治疗靶点提供了新的见解。试验注册本研究已在南京医科大学第一附属医院伦理委员会注册（试验注册号：2012-SR-127，注册日期：2012年1月20日）本文的在线版本（10. 1186/s12935-018-0537-8）包含补充材料，可供授权用户使用。
Esophageal squamous cell carcinoma (ESCC) is one of the prevalent and deadly cancers worldwide, especially in China. Considering the poor prognosis of ESCC, the aim of this study is to dissect the effects of long non-coding RNA (lncRNA) AK001796 on cell proliferation and cell cycle in vitro and tumorigenicity in vivo, providing therapeutic targets for ESCC. We conducted quantitative real time PCR to detect the expression level of lncRNA AK001796 in human ESCC tumor and adjacent non-tumor tissues, and analyzed the correlation between lncRNA AK001796 expression and clinicopathologic feature of ESCC patients. Then we knocked down the expression of lncRNA AK001796 in human ESCC cell lines Eca-109 and TE-1, and next inspected cell cycle and apoptosis condition in these cells using flow cytometry. Subsequently, we used CCK-8 assay to test proliferation ability of the lncRNA AK001796-silenced ESCC cells, and the MDM2/p53 signaling pathway in these cells was analyzed by western blot analysis. At last, the ESCC xenograft models were established to verify the role of lncRNA AK001796 on the occurrence and development of ESCC. In this study, we demonstrated that lncRNA AK001796 was significantly upregulated in ESCC tumor tissues compared to adjacent non-tumor tissues. Knockdown of lncRNA AK001796 inhibited ESCC cell growth, cell cycle, and tumor growth in a xenograft mouse model via regulating MDM2/p53 signal pathway. The expression of lncRNA AK001796 was positively correlated with MDM2 levels in human ESCC samples. Overall, lncRNA AK001796 regulates cell proliferation and cell cycle via modulating MDM2/p53 signaling in ESCC, which provides a new insight into the treatment targets for ESCC. Trial registration This study was registrated in the Ethics Committee of the First Affiliated Hospital of Nanjing Medical University (Trial registration: 2012-SR-127, Registered 20 January 2012) The online version of this article (10.1186/s12935-018-0537-8) contains supplementary material, which is available to authorized users.
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