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Abstract
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.
Highlights
Nasopharyngeal carcinoma (NPC) is a disease highly sensitive to radiotherapy with the unclear etiology
Venn analysis of the four microarray data was conducted to further obtain differentially expressed gene (DEG) in NPC (Figure 1E), revealing that 22 genes existed in the intersection of the four microarray data, which were all differentially expressed in the four NPC-related microarray data
Results of ethynyl-2 -deoxyuridine (EdU) assay for the detection of cell proliferation of HONE1 and CNE1 cells after transfection showed that compared with the blank group, there was no obvious difference in cell proliferation in the negative control (NC)-mimic group and si-NC group (P>0.05), but cell proliferation was significantly reduced in the LY294002 group (P
Summary
Nasopharyngeal carcinoma (NPC) is a disease highly sensitive to radiotherapy with the unclear etiology. 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-caspase. Nasopharyngeal carcinoma (NPC), a highly malignant squamous cell carcinoma originating from epithelial cells and occurring in the nasopharynx, is associated with distant metastasis and local invasion [1]. This cancer is geographically and ethnically distributed, mostly in southern China, especially in the Cantonese area around Guangzhou [2,3]. It is in urgent need to develop new biomarkers for NPC treatment
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