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

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.

SUBMITTER: Wang J

PROVIDER: S-EPMC7541952 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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

Wang Jianchu J Wang Wei W Tang Qianli Q Lu Libai L Luo Zongjiang Z Li Wenchuan W Lu Yuan Y Pu Jian J

Frontiers in genetics 20200924

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 ...[more]

PMID: 33193591

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Project description:BackgroundRecently, it has been reported that long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2), a novel tumor suppressor, participates in regulating the carcinogenesis and suppresses tumor progression by sponging microRNAs (miRNAs). However, the expression and function of CASC2 in hepatocellular carcinoma (HCC) remain unclear.MethodsThe expression of CASC2 and miR-367 in HCC specimens and cell lines were detected by real-time PCR. Western blotting and immunohistochemistry were carried out for detection of epithelial-to-mesenchymal transition (EMT) markers in HCC. Transwell assays were used to determine migration and invasion of HCC cells. A mouse model for lung metastasis was established to evaluated HCC metastasis in vivo. The correlation among CASC2, miR-367 and F-box and WD repeat domain containing 7 (FBXW7) were disclosed by a dual-luciferase reporter assay, RIP assay and biotin pull-down assay.ResultsHere, CASC2 expression was significantly downregulated in HCC tissues, especially in aggressive and recurrent cases. In accordance, CASC2 underexpression was observed in HCC cell lines compared to LO2. In vitro and in vivo experiments revealed that CASC2 inhibited migration and invasion of HCC cells. Additionally, CASC2 repressed EMT process of HCC cells. Further studies demonstrated that CASC2 could function as a competing endogenous RNA (ceRNA) by sponging miR-367 in HCC cells. Functionally, gain- and loss-of-function studies showed that miR-367 promoted migration, invasion and EMT progression of HCC cells. Moreover, further investigations disclosed that FBXW7 was a downstream target of miR-367 and CASC2 prohibited EMT progression and subsequently exerted its anti-metastatic effects via CASC2/miR-367/FBXW7 axis in HCC cells. Clinically, CASC2 underexpression and miR-367 overexpression were closely correlated with the metastasis-associated clinicopathologic features. Notably, CASC2 low-expressing and miR-367 high-expressing HCC patients showed the poorest clinical outcome.ConclusionsOverall, we conclude that the CASC2/miR-367/FBXW7 axis may be a ponderable and promising therapeutic target for HCC.

Dataset Information

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

Publications

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

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