Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Background: Nasopharyngeal carcinoma (NPC) is a disease highly sensitive to radiotherapy with the unclear etiology. However, the specific effects of microRNA-613 (miR-613) on NPC still remain elusive. Therefore, the present study probes into the underlying mechanism of miR-613 in NPC via AKT signaling pathway by regulating Fibronectin 1 (FN1).Methods: First, microarray analysis was used to screen differentially expressed genes (DEGs) and regulatory miRs associated with NPC. Next, miR-613 and FN1 expression in NPC cells was determined, followed by verification of target relationship between miR-613 and FN1. With NPC cells exposed to miR-613 mimic, si-FN1 and LY294002 (inhibitor of AKT signaling pathway), the regulatory effects of miR-613 on proliferation, apoptosis, invasion, migration and angiogenesis of NPC cells were detected with ratio of B-cell lymphoma 2/Bcl-2-associated X protein (Bcl-2/Bax), Cleaved-caspase3, matrix metallopeptidase 2 (MMP-2), MMP-9, vascular endothelial growth factor (VEGF), and cell adhesion molecule-1 (CD31) expression measured. Then, tumorigenesis and MVD were determined after Xenograft in nude mice.Results: FN1 modulated by miR-613 was critical for NPC via the AKT signaling pathway. NPC cells exhibited down-regulated miR-613 and up-regulated FN1. Besides, miR-613 was verified to target FN1. Moreover, overexpressed miR-613, silenced FN1 or LY294002 treatment suppressed proliferation, invasion, migration, and angiogenesis in NPC cells, which was indicated by reduced expression of AKT, mTOR, MMP-2, MMP-9, VEGF, and CD31 as well as decreased ratio of Bcl-2/Bax and increased expression of Cleaved-caspase3. Furthermore, cell apoptosis was promoted and tumorigenesis and MVD in nude mice were inhibited with overexpression of miR-613, silenced FN1 or LY294002 treatment.Conclusion: Taken together, miR-613 inhibits angiogenesis in NPC cells through inactivating FN1-dependent AKT signaling pathway.
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PMID:microRNA-613 exerts anti-angiogenic effect on nasopharyngeal carcinoma cells through inactivating the AKT signaling pathway by down-regulating FN1. 3261 60