文献类型：期刊文献

英文题名：CircHIPK3/miR-381-3p axis modulates proliferation, migration, and glycolysis of lung cancer cells by regulating the AKT/mTOR signaling pathway

作者：Gu, Feng[2];Zhang, Junhan[3];Yan, Lin[4];Li, Dong[1]

第一作者：Gu, Feng

通信作者：Li, D[1]

机构：[1]Gansu Prov Tumor Hosp, Dept Thorac Surg, 2 Xiaoxihu East St, Lanzhou, Gansu, Peoples R China;[2]Gansu Prov Tumor Hosp, Dept Aspirat Oncol, Lanzhou, Gansu, Peoples R China;[3]Gansu Univ Chinese Med, Dept Res & Expt Ctr, Lanzhou, Gansu, Peoples R China;[4]Gansu Prov Hosp, Dept Anesthesiol, Lanzhou, Gansu, Peoples R China

第一机构：Gansu Prov Tumor Hosp, Dept Thorac Surg, 2 Xiaoxihu East St, Lanzhou, Gansu, Peoples R China

通信机构：[1]corresponding author), Gansu Prov Tumor Hosp, Dept Thorac Surg, 2 Xiaoxihu East St, Lanzhou, Gansu, Peoples R China.

年份：2020

卷号：15

期号：1

起止页码：683

外文期刊名：OPEN LIFE SCIENCES

收录：;Scopus(收录号：2-s2.0-85093696971);WOS:【SCI-EXPANDED(收录号:WOS:000569754900001)】；

语种：英文

外文关键词：lung cancer; circHIPK3; miR-381-3p; glycolysis; AKT/mTOR signaling pathway

摘要：Lung cancer is a lethal malignancy. Plenty of circular RNAs (circRNAs) have been identified to be the vital regulators in lung cancer development. Here, we intended to clarify the functional role of circRNA HIPK3 (circHIPK3, also called hsa_circ_0021593) and its underlying mechanism of action. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was employed to evaluate the levels of circHIPK3 and miR-381-3p. Cell viability and apoptosis rate were monitored by Cell Counting Kit-8 assay and flow cytometry, respectively. Cell migration was estimated through the Transwell assay. To assess glycolysis, commercial kits were utilized to measure the levels of glucose and lactate and the enzyme activity of hexokinase-2 (HK2). Expression of related proteins was detected via western blot analysis. The target connection between circHIPK3 and miR-381-3p was validated by dual-luciferase reporter, RIP, and pull-down assays. The role of circHIPK3 in vivo was determined via the xenograft assay. CircHIPK3 was upregulated, while miR-381-3p was downregulated in lung cancer tissues and cells. And circHIPK3 deficiency inhibited lung cancer progression by lowering cell proliferation, migration, glycolysis, and promoting apoptosis of lung cancer cells in vitro. MiR-381-3p was a target of circHIPK3, and miR-381-3p interference alleviated circHIPK3 knockdown-induced lung cancer progression inhibition. CircHIPK3 could activate the protein kinase B/mammalian target of rapamycin (AKT/mTOR) signaling pathway. Moreover, circHIPK3 knockdown suppressed tumor growth in vivo by inactivating the AKT/mTOR signaling pathway. In conclusion, the silencing of circHIPK3 inhibited lung cancer progression, at least in part, by sponging miR-381-3p and inactivating the AKT/mTOR signaling pathway.