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长链基因间非编码RNA 00152在胰腺癌糖酵解中的作用：对微小RNA-185-5p/类 Kruppel样因子7轴的调控

Role of long intergenic non-protein coding RNA 00152 in pancreatic cancer glycolysis the manipulation of the microRNA-185-5p/Krüppel-like factor 7 axis.

作者信息

Li Haifeng, Shen Hao, Xie Peng, Zhang Zheng, Wang Lishan, Yang Yang, Yu Zeqian, Cheng Zhangjun, Zhou Jiahua

机构信息

Department of Hepato-Pancreatico-Biliary Surgery, Zhongda Hospital, Medical School, Southeast University, 87 Dingjiaqiao Road, Nanjing, 210009, Jiangsu Province, China.

Department of Hepato-Pancreatico-Biliary Surgery, Zhongda Hospital Southeast University, Nanjing, 210009, Jiangsu Province, China.

出版信息

J Cancer. 2021 Aug 28;12(21):6330-6343. doi: 10.7150/jca.63128. eCollection 2021.

DOI:10.7150/jca.63128
PMID:34659523
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8489139/
Abstract

The current study set out to investigate the role of long intergenic non-protein coding RNA (LINC) 00152 in pancreatic cancer (PC) cell glycolysis with the microRNA (miR)-185-5p/Krüppel-like factor 7 (KLF7) axis. Firstly, PC tissues and cells as well as the control ones were collected from 53 PC patients, and assessed for LINC00152 expression patterns. Besides, PC cells with the most differentially expressed LINC00152 were selected for further experiments. When LINC00152 was silenced or overexpressed, PC cell glucose consumption, lactic acid production, adenosine triphosphate and levels of glycolysis-associated enzymes were detected. In addition, the binding relation between LINC00152 and miR-185-5p as well as the target relation between miR-185-5p and KLF7 was clarified and validated. Additionally, xenograft transplantation was performed to confirm the experiments. It was found that LINC00152 was over-expressed in PC, and it predicted a poor prognosis. Besides, LINC00152 knockdown inhibited PC cell glycolysis. Moreover, LINC00152 could specifically targeted miR-185-5p. Meanwhile, LINC00152 exhaustion blocked PC cell glycolysis through the up-regulation of miR-185-5p. Lastly, LINC00152 inhibition targeted miR-185-5p to quench KLF7, therefore suppressing PC cell tumorigenesis and glycolysis. Collectively, our findings indicated that silencing LINC00152 restricted PC cell glycolysis promoting miR-185-5p and reducing KLF7.

摘要

本研究旨在探讨长链基因间非编码RNA（LINC）00152在胰腺癌（PC）细胞糖酵解过程中通过微小RNA（miR）-185-5p/类 Kruppel 样因子 7（KLF7）轴所发挥的作用。首先，收集了53例PC患者的PC组织、细胞以及对照组织和细胞，并评估LINC00152的表达模式。此外，选择LINC00152表达差异最大的PC细胞进行进一步实验。当LINC00152被沉默或过表达时，检测PC细胞的葡萄糖消耗、乳酸生成、三磷酸腺苷以及糖酵解相关酶的水平。另外，明确并验证了LINC00152与miR-185-5p之间的结合关系以及miR-185-5p与KLF7之间的靶向关系。此外，进行了异种移植实验以证实上述实验结果。研究发现，LINC00152在PC中过表达，且预示着预后不良。此外，敲低LINC00152可抑制PC细胞糖酵解。而且，LINC00152可特异性靶向miR-185-5p。同时，LINC00152缺失通过上调miR-185-5p来阻断PC细胞糖酵解。最后，抑制LINC00152靶向miR-185-5p以抑制KLF7，从而抑制PC细胞的肿瘤发生和糖酵解。总的来说，我们的研究结果表明，沉默LINC00152可通过促进miR-185-5p和降低KLF7来限制PC细胞糖酵解。

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