Long Non-coding RNA lnc-GNAT1-1 Suppresses Liver Cancer Progression via Modulation of Epithelial–Mesenchymal Transition

Wang, Jianchu and Wang, Wei and Tang, Qianli and Lu, Libai and Luo, Zongjiang and Li, Wenchuan and Lu, Yuan and Pu, Jian (2020) Long Non-coding RNA lnc-GNAT1-1 Suppresses Liver Cancer Progression via Modulation of Epithelial–Mesenchymal Transition. Frontiers in Genetics, 11. ISSN 1664-8021

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Abstract

Recent studies have investigated the modulatory roles of long non-coding RNAs in the onset and progression of liver cancer. The present study aimed to elucidate the role of lnc-GNAT1-1 in liver cancer development and to explore the underlying mechanisms. Quantitative real-time polymerase chain reaction was performed to measure the expression levels of lnc-GNAT1-1 in cancerous tissues from patients with liver cancer and in liver cancer cell lines. The proliferative ability and apoptotic rates of liver cancer cells were measured using the counting kit-8 (CCK-8), colony formation, and flow cytometry assays. The abilities to invade and migrate were measured using Transwell assays. Epithelial–mesenchymal transition (EMT)-related proteins, E-cadherin, N-cadherin, and vimentin, were measured using western blotting. A nude mouse model was injected with xenografts to evaluate tumor growth in vivo. Downregulation of lnc-GNAT1-1 was observed in cancerous tissues from patients with liver cancer and in liver cancer cell lines, and low expression levels of lnc-GNAT1-1 were related to advanced TNM stage. Lnc-GNAT1-1 knockdown promoted invasion, migration, and proliferation of liver cancer cells and inhibited apoptosis, while lnc-GNAT1-1 upregulation exerted the opposite effects. The expression levels of lnc-GNAT1-1 negatively correlated with in vivo tumor growth in a xenograft nude mouse model. Mechanistic experiments revealed that lnc-GNAT1-1 exerted anti-tumor effects in liver cancer cells by inhibiting EMT. In conclusion, this study suggests that lnc-GNAT1-1 suppresses liver cancer progression by modulating EMT.

Item Type: Article
Subjects: GO for STM > Medical Science
Depositing User: Unnamed user with email support@goforstm.com
Date Deposited: 11 Sep 2023 09:25
Last Modified: 11 Sep 2023 09:25
URI: http://archive.article4submit.com/id/eprint/1384

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