RESUMO
PURPOSE: To investigate the regulation of long non-coding RNA (LncRNA) RUNX1-IT1 on microrna (mir-195)/CyclinD1 (CyclinD1) in malignant pleomorphic adenoma (MPA). METHODS: The MPA tissues and para-carcinoma tissues were collected and the expression levels of LncRNA RUNX1-IT1, miR-195 and CyclinD1 mRNA were detected, the correlation and clinical pathology of MPA was analyzed and compared. MPA cell line SM-AP1 was cultured and transfected with negative control(NC) siRNA, LncRNA RUNX1-IT1siRNA, miR-NC and miR-195 inhibitor. Cell proliferation level A490 and expression levels of miR-195 and CyclinD1 were detected. LncRNA RUNX1-IT1 targeting miR-195 and miR-195 targeting CyclinD1 were analyzed by dual luciferase reporter gene assay. SPSS 21.0 software package was used for data analysis. RESULTS: The expression level of LncRNA RUNX1-IT1 and CyclinD1 in MPA were higher than those in para tumor tissues, and the expression level of miR-195 was lower than that in para tumor tissues(Pï¼0.05). LncRNA RUNX1-IT1was negatively correlated with miR-195, positively correlated with CyclinD1, and miR-195 was negatively correlated with CyclinD1. The expression of LncRNA RUNX1-IT1 and CyclinD1 in MPA tissue with tumor diameter≥3 cm, recurrence and distant metastasis increased(Pï¼0.05), while the expression of miR-195 decreased(Pï¼0.05). After knockdown of LncRNA RUNX1-IT1, A490 level and CyclinD1 expression level decreased, while miR-195 expression level increased(Pï¼0.05). miR-195 decreased the fluorescence activity of LncRNA RUNX1-IT1 and CyclinD1 reporter genes(Pï¼0.05). After miR-195 was inhibited, the effect of LncRNA RUNX1-IT1 knockdown on decreasing A490 level and CyclinD1 expression level weakened(Pï¼0.05). CONCLUSIONS: LncRNA RUNx1-IT1 may participate in the development of MPA by regulating the expression of miR-195/CyclinD1.
Assuntos
Adenoma Pleomorfo , MicroRNAs , RNA Longo não Codificante , Neoplasias das Glândulas Salivares , Humanos , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Neoplasias das Glândulas Salivares/genéticaRESUMO
Retinoic acid-inducible gene I (RIG-I) is a pattern recognition receptor and is involved in the innate immune response against RNA viruses infection. Here, we demonstrate that the Ras-GTPase-activating protein SH3-domain-binding protein 1 (G3BP1) serves as a positive regulator of the RIG-I-mediated signaling pathway. G3BP1-deficient cells inhibited RNA virus-triggered induction of downstream antiviral genes. Furthermore, we found that G3BP1 inhibited the replication of Sendai virus and vesicular stomatitis virus, indicating a positive regulation of G3BP1 to cellular antiviral responses. Mechanistically, G3BP1 formed a complex with RNF125 and RIG-I, leading to decreased RNF125 via its auto-ubiquitination; thus, promoting expression of RIG-I. Overall, the results suggest a novel mechanism for G3BP1 in the positive regulation of antiviral signaling mediated by RIG-I.