Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1384489 (Scratch)
 395 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BACKGROUND Let-7 microRNAs (miRNAs) have the effects of inhibiting tumor growth and metastasis, however, the research in nasopharyngeal carcinoma (NPC) is limited. This study focused on the effects of Let-7 on NPC migration and invasion and the mechanism of action. MATERIAL AND METHODS Plasmid transfection was used to upregulate the expression levels of Let-7g-5p and insulin-like growth factor-1 receptor (IGF-1R). Cell counting kit-8 (CCK-8) assay was applied to test the cell viability. Scratch assay and Transwell assay were performed to detect the migration and invasion abilities. Bioinformatics prediction and luciferase reporter assay were used to determine and verify the downstream target genes for Let-7g-5p. Protein and mRNA were detected by western blot and real-time quantitative polymerase chain reaction (RT-qPCR), respectively. RESULTS Let-7g-5p was under-expressed in human NPC cells. Overexpression of Let-7g-5p could inhibit cell viability and inhibit the migration and invasion of SUNE1 cells. The dual-luciferase reporter assay showed that IGF-1R was a direct target gene of Let-7g-5p, which was directly regulated IGF-1R expression by 3'UTR. Let-7g-5p overexpression could inhibit the expression of IGF-1R gene, and upregulation of IGF-1R gene expression reversed the inhibitory effect of Let-7g-5p on cell viability and epithelial-mesenchymal transition processes. CONCLUSIONS Let-7g-5p is lowly expressed in NPC and it was the first to discover that IGF-1R was a target gene of let-7g-5p in NPC. Upregulation of IGF-1R reversed the inhibitory effect of Let-7g-5p on epithelial-mesenchymal transition.
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PMID:Upregulation of Insulin-Like Growth Factor-1 Receptor (IGF-1R) Reverses the Inhibitory Effect of Let-7g-5p on Migration and Invasion of Nasopharyngeal Carcinoma. 3137 70

Preeclampsia (PE) is a pregnancy-specific syndrome that substantially leads to maternal and fetal mortality. Multiple factors contribute to the disease, but the exact pathogenesis still remains elusive. Here we explored the roles of lncRNA MALAT1 and miR-206 in PE. qRT-PCR was applied to measure mRNA levels of MALAT1 and miR-206 in the placenta of PE patients. Scratch wound healing assay and transwell invasion assay were conducted to test the effects of MALAT1 and miR-206 on migration and invasion of trophoblast cells. In addition, we validated MALAT1/miR-206 and miR-206/IGF-1 interactions with dual luciferase reporter assay. Western bot was used to detect protein expressions of IGF-1, p-PI3K, PI3K, p-Akt and Akt. We found that MALAT1 was decreased but miR-206 was increased in the placenta of patients with PE. Inhibition of MALAT1, knockdown IGF-1, or miR-206 mimics suppressed the trophoblast cells migration and invasion, while overexpression of MALAT1, IGF-1 or miR-206 inhibitors exhibited opposite effects. Further, miR-206 was confirmed as a direct target of MALAT1. Besides, miR-206 inhibited IGF-1 expression by directly binding to the 3'UTR. Mechanistically, our study demonstrated that MALAT1 regulates IGF-1/PI3K/Akt signaling via miR-206. Together, these results suggest that MALAT1 and miR-206 play important roles in PE. MALAT1 regulates miR-206/IGF-1 axis, thereby modulating trophoblast cells migration and invasion through PI3K/Akt signal pathway. These results show light on the underlying mechanisms of PE and provide potential targets for PE therapy.Abbreviations: PE: Preeclampsia; lncRNA: Long-non-coding RNA; MALAT1: Metastasis-associated lung adenocarcinoma transcript 1; IGF-1: Insulin-like growth factor 1; PI3k: Phosphatidylinositol-4, 5-bisphosphate 3-kinase; Akt: Protein kinase B; GAPDH: Glyceraldehyde 3-phosphate dehydrogenase; qRT-PCR: Quantitative Reverse Transcription polymerase chain reaction; shRNA: Short hairpin RNA; siRNA: Small interfering RNA; EMT: Epithelial-mesenchymal transition.
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PMID:LncRNA MALAT1 regulates trophoblast cells migration and invasion via miR-206/IGF-1 axis. 3177 73