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MiR-424-5p reversed epithelial-mesenchymal transition of anchorage-independent HCC cells by directly targeting ICAT and suppressed HCC progression.
Sci Rep. 2014 Sep 01; 4:6248.SR

Abstract

Resistance to anoikis and Epithelial-mesenchymal transition (EMT) are two processes critically involved in cancer metastasis. In this study, we demonstrated that after anchorage deprival, hepatocellular carcinoma (HCC) cells not only resisted anoikis, but also exhibited EMT process. Microarray expression profiling revealed that expression of miR-424-5p was significantly decreased in anoikis-resistant HCC cells. Ectopic overexpression of miR-424-5p was sufficient to reverse resistance to anoikis, block EMT process and inhibit malignant behaviors of HCC cells. Target analysis showed that a potent β-catenin inhibitor, ICAT/CTNNBIP1 was a direct target of miR-424-5p. Further study demonstrated that miR-424-5p reversed resistance to anoikis and EMT of HCCs by directly targeting ICAT and further maintaining the E-cadherin/β-catanin complex on the cellular membrance. In vivo study further demonstrated that miR-424-5p significantly inhibited the tumorigenicity of HCC cells in nude mice. Clinical investigation demonstrated that miR-424-5p was significantly downregulated in HCC tissues compared with that of the non-cancerous liver tissues, and this decreased expression of miR-424-5p was significantly correlated with higher pathological grades and more advanced TNM stages. Therefore, aberrant expression of miR-424-5p is critically involved in resistance to anoikis and EMT during the metastatic process of HCC, and its downregulation significantly contributes to liver cancer progression.

Authors+Show Affiliations

Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.Department of Gastroenterology, Provincial Hospital Affiliated with Shandong University, Jinan 250021, China.Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.Department of Gastroenterology, Shandong University Qilu Hospital, Jinan 250012, China.Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.Department of Immunology, Shandong University School of Medicine, Jinan 250012, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25175916

Citation

Zhang, Ying, et al. "MiR-424-5p Reversed Epithelial-mesenchymal Transition of Anchorage-independent HCC Cells By Directly Targeting ICAT and Suppressed HCC Progression." Scientific Reports, vol. 4, 2014, p. 6248.
Zhang Y, Li T, Guo P, et al. MiR-424-5p reversed epithelial-mesenchymal transition of anchorage-independent HCC cells by directly targeting ICAT and suppressed HCC progression. Sci Rep. 2014;4:6248.
Zhang, Y., Li, T., Guo, P., Kang, J., Wei, Q., Jia, X., Zhao, W., Huai, W., Qiu, Y., Sun, L., & Han, L. (2014). MiR-424-5p reversed epithelial-mesenchymal transition of anchorage-independent HCC cells by directly targeting ICAT and suppressed HCC progression. Scientific Reports, 4, 6248. https://doi.org/10.1038/srep06248
Zhang Y, et al. MiR-424-5p Reversed Epithelial-mesenchymal Transition of Anchorage-independent HCC Cells By Directly Targeting ICAT and Suppressed HCC Progression. Sci Rep. 2014 Sep 1;4:6248. PubMed PMID: 25175916.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MiR-424-5p reversed epithelial-mesenchymal transition of anchorage-independent HCC cells by directly targeting ICAT and suppressed HCC progression. AU - Zhang,Ying, AU - Li,Tao, AU - Guo,Pengbo, AU - Kang,Jia, AU - Wei,Qing, AU - Jia,Xiaoqing, AU - Zhao,Wei, AU - Huai,Wanwan, AU - Qiu,Yumin, AU - Sun,Lei, AU - Han,Lihui, Y1 - 2014/09/01/ PY - 2014/01/20/received PY - 2014/08/12/accepted PY - 2014/9/2/entrez PY - 2014/9/2/pubmed PY - 2015/10/17/medline SP - 6248 EP - 6248 JF - Scientific reports JO - Sci Rep VL - 4 N2 - Resistance to anoikis and Epithelial-mesenchymal transition (EMT) are two processes critically involved in cancer metastasis. In this study, we demonstrated that after anchorage deprival, hepatocellular carcinoma (HCC) cells not only resisted anoikis, but also exhibited EMT process. Microarray expression profiling revealed that expression of miR-424-5p was significantly decreased in anoikis-resistant HCC cells. Ectopic overexpression of miR-424-5p was sufficient to reverse resistance to anoikis, block EMT process and inhibit malignant behaviors of HCC cells. Target analysis showed that a potent β-catenin inhibitor, ICAT/CTNNBIP1 was a direct target of miR-424-5p. Further study demonstrated that miR-424-5p reversed resistance to anoikis and EMT of HCCs by directly targeting ICAT and further maintaining the E-cadherin/β-catanin complex on the cellular membrance. In vivo study further demonstrated that miR-424-5p significantly inhibited the tumorigenicity of HCC cells in nude mice. Clinical investigation demonstrated that miR-424-5p was significantly downregulated in HCC tissues compared with that of the non-cancerous liver tissues, and this decreased expression of miR-424-5p was significantly correlated with higher pathological grades and more advanced TNM stages. Therefore, aberrant expression of miR-424-5p is critically involved in resistance to anoikis and EMT during the metastatic process of HCC, and its downregulation significantly contributes to liver cancer progression. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/25175916/MiR_424_5p_reversed_epithelial_mesenchymal_transition_of_anchorage_independent_HCC_cells_by_directly_targeting_ICAT_and_suppressed_HCC_progression_ L2 - https://doi.org/10.1038/srep06248 DB - PRIME DP - Unbound Medicine ER -