T-T Gong1, F-Z Sun, J -Y Chen, J-F Liu, Y Yan, D Li, B Zhou, H Shan. 1. Department of Interventional Medicine, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China. 479782767@qq.com.
Abstract
OBJECTIVE: Hepatocellular carcinoma (HCC) is a common malignant tumor. Increasing evidence has demonstrated that microRNAs (miRNAs) play an important role in a wide variety of cellular processes. However, there are few reports about the role and underlying molecular mechanisms of miRNAs in HCC. PATIENTS AND METHODS: qRT-PCR and Western blots were performed to quantify the expression of miR-92a, E-cadherin, and circPTK2. Proliferation and invasion assays were performed to explore the function of miR-92a and circPTK2. A Luciferase assay was used to test the relationship between miR-92a, E-cadherin, and circPTK2. RESULTS: In this study, we found that miR-92a was upregulated in HCC tissues and HCC cell lines. Overexpression of miR-92a enhanced cell proliferation and invasion by targeting the E-cadherin 3'UTR in HCC cells. Furthermore, we found that circPTK2 inhibited EMT by inhibiting miR-92a, preventing its ability to downregulate E-cadherin in HCC cells. CONCLUSIONS: We identified a regulatory axis comprising circPTK2/miR-92a/E-cadherin in HCC cells that may serve as a valuable biomarker and therapeutic target for patients with HCC.
OBJECTIVE:Hepatocellular carcinoma (HCC) is a common malignant tumor. Increasing evidence has demonstrated that microRNAs (miRNAs) play an important role in a wide variety of cellular processes. However, there are few reports about the role and underlying molecular mechanisms of miRNAs in HCC. PATIENTS AND METHODS: qRT-PCR and Western blots were performed to quantify the expression of miR-92a, E-cadherin, and circPTK2. Proliferation and invasion assays were performed to explore the function of miR-92a and circPTK2. A Luciferase assay was used to test the relationship between miR-92a, E-cadherin, and circPTK2. RESULTS: In this study, we found that miR-92a was upregulated in HCC tissues and HCC cell lines. Overexpression of miR-92a enhanced cell proliferation and invasion by targeting the E-cadherin 3'UTR in HCC cells. Furthermore, we found that circPTK2 inhibited EMT by inhibiting miR-92a, preventing its ability to downregulate E-cadherin in HCC cells. CONCLUSIONS: We identified a regulatory axis comprising circPTK2/miR-92a/E-cadherin in HCC cells that may serve as a valuable biomarker and therapeutic target for patients with HCC.