G Zhang1, Y-J Wu, F Yan. 1. Department of Thoracic Surgery, The Seventh People's Hospital of Jinan, Jinan, China. yigehaoren321@163.com.
Abstract
OBJECTIVE: This study was designed to investigate whether microRNA-130-5p could promote the progression and metastasis of lung cancer by targeting enhancer of zeste homolog 2 (EZH2). PATIENTS AND METHODS: The level of microRNA-130-5p was examined in the tumor tissues and paracancerous tissues of lung adenocarcinoma patients. Meanwhile, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the level of microRNA-130-5p in different lung adenocarcinoma cell lines, which was found markedly decreased in two lung cancer cell lines. Moreover, microRNA-130-5p mimic and inhibitor were transfected in cells to achieve microRNA-130-5p overexpression and knockdown model to observe its effect on cell biological function. Cell Counting Kit-8 (CCK-8) assay was performed to detect cell viability, while transwell assay was used to detect cell invasion as well as migration. Subsequently, EZH2 was predicted as the target gene of microRNA-130-5p using the Bioscan prediction site Targetscan, which was confirmed by Luciferase reporter gene assay. Besides, the level of EZH2 was detected by qRT-PCR and Western blot after overexpression and knockdown of microRNA-130-5p. Finally, the combination of si-EZH2 and inhibitor was used to further verify whether microRNA-130-5p could promote cell metastasis and invasion of lung cancer by targeting EZH2. RESULTS: MicroRNA-130-5p expression in tumor tissues of patients with lung adenocarcinoma was markedly lower than that in normal tissues. Besides, microRNA-130-5p expression in tumor tissues with large diameter was lower than that with a small diameter. In addition, microRNA-130-5p was also lowly expressed in lung cancer cell lines. High expression of microRNA-130-5p reduced the cell viability and inhibited cancer cell metastasis and invasion. At the same time, microRNA-130-5p knockdown enhanced the activity of lung cancer cells and promoted cancer cell invasion as well as migraindicated confirmed that microRNA-130-5p could bind to EZH2. Additionally, the overexpression or knockdown of microRNA-130-5p could decrease or increase the levels of EZH2 mRNA, respectively. Finally, EZH2 silencing reduced lung cancer cell activity and inhibited cancer cells invasion as well as migration, which could be reversed by the microRNA-130-5p inhibitor. CONCLUSIONS: The reduced microRNA-130-5p expression in lung cancer tissues and cells promoted metastasis and invasion of this tumor by targeting EZH2.
OBJECTIVE: This study was designed to investigate whether microRNA-130-5p could promote the progression and metastasis of lung cancer by targeting enhancer of zeste homolog 2 (EZH2). PATIENTS AND METHODS: The level of microRNA-130-5p was examined in the tumor tissues and paracancerous tissues of lung adenocarcinomapatients. Meanwhile, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the level of microRNA-130-5p in different lung adenocarcinoma cell lines, which was found markedly decreased in two lung cancer cell lines. Moreover, microRNA-130-5p mimic and inhibitor were transfected in cells to achieve microRNA-130-5p overexpression and knockdown model to observe its effect on cell biological function. Cell Counting Kit-8 (CCK-8) assay was performed to detect cell viability, while transwell assay was used to detect cell invasion as well as migration. Subsequently, EZH2 was predicted as the target gene of microRNA-130-5p using the Bioscan prediction site Targetscan, which was confirmed by Luciferase reporter gene assay. Besides, the level of EZH2 was detected by qRT-PCR and Western blot after overexpression and knockdown of microRNA-130-5p. Finally, the combination of si-EZH2 and inhibitor was used to further verify whether microRNA-130-5p could promote cell metastasis and invasion of lung cancer by targeting EZH2. RESULTS: MicroRNA-130-5p expression in tumor tissues of patients with lung adenocarcinoma was markedly lower than that in normal tissues. Besides, microRNA-130-5p expression in tumor tissues with large diameter was lower than that with a small diameter. In addition, microRNA-130-5p was also lowly expressed in lung cancer cell lines. High expression of microRNA-130-5p reduced the cell viability and inhibited cancer cell metastasis and invasion. At the same time, microRNA-130-5p knockdown enhanced the activity of lung cancer cells and promoted cancer cell invasion as well as migraindicated confirmed that microRNA-130-5p could bind to EZH2. Additionally, the overexpression or knockdown of microRNA-130-5p could decrease or increase the levels of EZH2 mRNA, respectively. Finally, EZH2 silencing reduced lung cancer cell activity and inhibited cancer cells invasion as well as migration, which could be reversed by the microRNA-130-5p inhibitor. CONCLUSIONS: The reduced microRNA-130-5p expression in lung cancer tissues and cells promoted metastasis and invasion of this tumor by targeting EZH2.