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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Antigens, CD, Antineoplastic Agents, Phytogenic, Cadherins, Carcinoma, Hepatocellular, Cell Line, Tumor, Cell Movement, Collagenases, Diffusion Chambers, Culture, Epithelial-Mesenchymal Transition, Gene Expression Regulation, Neoplastic, Humans, Liver Neoplasms, NF-kappa B, Neoplasm Invasiveness, Nuclear Proteins, RANK Ligand, Receptor Activator of Nuclear Factor-kappa B, Sesquiterpenes, Signal Transduction, Snail Family Transcription Factors, Transcription Factors, Twist-Related Protein 1, Vimentin.
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Does rANKL promote migration and invasion of hepatocellular carcinoma cells via NF-κB-mediated epithelial-mesenchymal transition? Context: Metastasis accounts for the most deaths in patients with hepatocellular carcinoma (HCC). Receptor activator of nuclear factor kappa B ligand (RANKL) is associated with cancer metastasis, while its role in HCC remains largely unknown. Immunohistochemistry was performed to determine the expression of RANK in HCC tissue (n = 398). Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to examine the expression of RANK, E-cadherin, N-cadherin, vimentin, Snail, Slug, Twist and MMPs in HCC cells. Wound healing and Transwell assays were used to evaluate cell migration and invasion ability. We found that expression of RANK, the receptor of RANKL, was significantly higher in HCC tumor tissues than in peritumor liver tissues (p<0.001). Constitutive expression of RANK was detected in HCC cell lines, which can be up-regulated when HCC cells were stimulated with RANKL. Notably, in vitro experiments showed that activation of RANKL-RANK axis significantly promoted migration and invasion ability of HCC cells. In addition, RANKL stimulation increased the expression levels of N-cadherin, Snail, and Twist, while decreased the expression of E-cadherin, with concomitant activation of NF-κB signaling pathway. Moreover, administration of the NF-κB inhibitor attenuated RANKL-induced migration, invasion and epithelial-mesenchymal transition of HCC cells.
assistant
RANKL could potentiate migration and invasion ability of RANK-positive HCC cells through NF-κB pathway-mediated epithelial-mesenchymal transition, which means that RANKL-RANK axis could be a potential target for HCC therapy. Final Decision: yes