Abstract
Interleukin-23 (IL-23) is a conventional proinflammatory cytokine that plays a role in tumor progression by inducing inflammation in the tumor microenvironment. However, the role of IL-23 in thyroid cancer migration and invasion remains unclear. In the present study, we observed that the treatment with IL-23, induced migration and invasion in human thyroid cancer cells. Additional data demonstrate that SOCS4 negatively regulates IL-23-mediated migration and invasion. On investigating the mechanisms involved in IL-23 mediated migration and invasion, we observed that miR-25 promotes the migration and invasion of thyroid cancer cells by directly binding to the 3'-UTR of SOCS4 that leads to the inhibition of SOCS4. In addition, we also demonstrated that IL-23 increases miR-25 expression levels, and overexpressed miR-25 is involved in IL-23-associated SOCS4 inhibition and cell migration and invasion. Together, our data suggest that IL-23 induces migration and invasion in thyroid cancer cells by mediating the miR-25/SOCS4 signaling pathway.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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3' Untranslated Regions
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Adult
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Cell Movement / drug effects
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DNA, Neoplasm / metabolism
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Female
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Gene Expression Regulation, Neoplastic / genetics
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Gene Expression Regulation, Neoplastic / physiology
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Humans
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Interleukin-23 / pharmacology*
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Male
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MicroRNAs / physiology*
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Middle Aged
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Neoplasm Invasiveness / physiopathology*
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RNA, Small Interfering / genetics
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Real-Time Polymerase Chain Reaction
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Signal Transduction
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Suppressor of Cytokine Signaling Proteins / biosynthesis
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Suppressor of Cytokine Signaling Proteins / genetics
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Suppressor of Cytokine Signaling Proteins / physiology*
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Thyroid Neoplasms / pathology*
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Tumor Cells, Cultured
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Up-Regulation
Substances
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3' Untranslated Regions
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DNA, Neoplasm
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Interleukin-23
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MIRN25 microRNA, human
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MicroRNAs
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RNA, Small Interfering
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SOCS4 protein, human
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Suppressor of Cytokine Signaling Proteins
Grants and funding
This work was supported by the grants from the National Natural Science Foundation of China (No.81372880); the Independent research project of Wuhan University (No. 2042014kf0184; NO. 2042014kf0119); the doctoral program of Higher Education Research Fund (No. 20130141120093; No. 20110141110062); the Natural Science Foundation of Hubei province (No.2012FFA045). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.