Background: Cholangiocarcinoma (CCA) is one of the most common primary biliary malignant tumors with a high mortality. MIR22HG has been reported to act as a tumor-suppressor gene in several types of cancers. However, the role and molecular regulatory mechanism of MIR22HG in CCA still remains unclear. The present study aimed to investigate the role and underlying mechanism of MIR22HG in CCA. Methods:The expression of MIR22HG was detected by RT-qPCR assayin CCA tissues and cells. CCK-8, colony formation and transwell assays were performed to study the biological function of MIR22HG in CCA. Western blot and immunofluorescence assays were performed to detect the expression ofWnt/β-catenin signaling pathway markers. In vivo assays were conducted to explore the biological role of MIR22HG. Results:We first found that MIR22HG expression was significantly downregulated in CCA tissues and cell lines. Moreover, MIR22HG expression was related to TNM stage and bore prognostic significance in CCA patients. Function experiments demonstrated that overexpression of MIR22HG inhibited cell proliferation, migration and invasion in CCA, whereas knockdown of MIR22HG caused the opposite result. It was found that MIR22HG negatively regulated mRNA and the expression levels of proteins in the Wnt/β-catenin signaling pathway (β-catenin, cyclin D1 and c-myc).The effect of MIR22HG overexpression on CCA progression could be partly rescued by activating the Wnt/β-catenin signaling pathway. MIR22HG suppressed CCA tumorigenesis in vivo. Conclusions:In summary, the results of the present study show that MIR22HG repressed cell proliferation, migration and invasion in CCA by negatively regulating the Wnt/β-catenin signaling pathway. MIR22HG may be a novel target for diagnosis and therapy in CCA.
Endothelial integrity or homeostasis is not only essential for regulating arterial activity and vascular tone under physiological conditions, but also critical for triggering various cardiovascular diseases including atherosclerosis and balloon angioplasty if such a balance has been impaired. Moreover, endothelial cell development and differentiation are key steps during embryogenesis and involves co-ordinations of diverse signaling molecules and transcription factors. Therefore, characterizing the molecular mechanisms underlying endothelial differentiation and development will not only improve our understanding of pathogenesis of vascular disease, but also facilitate our ability in generation of vessels cells from pluripotent stem cells for therapeutic purpose. MicroRNAs, a class of small, non-coding RNAs, have been extensively implicated in the regulation of various aspects of biological processes such as embryonic development, tissue/organ homeostasis, and metabolism, as well as almost all the human disease, particularly cancers and cardiovascular diseases. Accumulating evidence has implicated that microRNAs play an important role in regulation of endothelial development, phenotype and function. In this review, we will summarize new findings from recent studies in this field and discuss our current understanding of how microRNAs regulate endothelial development and differentiation from stem cells.
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