Background: Recently, long non-coding RNAs (lncRNAs) have been elucidated to play essential roles in cancers, and the recognition of lncRNA expression patterns in nasopharyngeal carcinoma (NPC) may be helpful for indicating novel mechanisms underlying NPC carcinogenesis. Herein, we conducted this study to probe into the function of lncRNA ZNF667-AS1 in NPC progression with the involvement of microRNA-1290 (miR-1290) and actin-binding LIM protein 1 (ABLIM1). Materials and Methods: In silico analysis screened differentially expressed genes and miRNAs in NPC and predicted potential mechanisms. ZNF667-AS1 expression was detected in NPC tissues and cells. The gain-and-loss function assays were performed to explore the effects of lncRNA ZNF667-AS1 and miR-1290 in NPC cell biological behaviors. In vivo experiments were further conducted to confirm the in vitro results. Results: In silico analysis predicted that ZNF667-AS1 was diminished in NPC, which may downregulate ABLIM1 through sponging miR-1290. ZNF667-AS1 was poorly expressed in NPC tissues and cells, and overexpression of ZNF667-AS1 inhibited growth of NPC cells. ZNF667-AS1 competitively bound with miR-1290, thereby upregulating ABLIM1. miR-1290 resulted in the promotion of NPC cell progression by suppressing ABLIM1. Overexpression of ZNF667-AS1 or suppression of miR-1290 inhibited tumorigenicity of NPC cells in vivo. Conclusion: This study highlights that lncRNA ZNF667-AS1 promotes ABLIM1 expression by sponging miR-1290 to suppress NPC cell progression.

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MicroRNA-30a (miR-30a) was previously reported to serve as a tumor suppressor able to inhibit the development and progression of certain types of cancer. A number of previous studies demonstrated that zinc finger E-box binding homeobox 2 (ZEB2) may be regulated by miR-30a in clear cell renal cell carcinoma and breast cancer. However, the function of miR-30a in human nasopharyngeal carcinoma (NPC) remains unclear. The present study aimed to investigate the association between miR-30a and ZEB2 in NPC. Therefore, the expression levels of miR-30a and ZEB2 were measured in human NPC cells and tissues from patients with NPC, and the present results suggested that the expression level of miR-30a was significantly decreased in NPC tissues compared with paracancerous tissues. The direct interaction between miR-30a and the untranslated region of ZEB2 was examined using the dual-luciferase reporter assay, and ZEB2 was identified as a direct target of miR-30a. Additionally, the effects of miR-30a and ZEB2 overexpression on cell proliferation, migration, invasion and apoptosis were additionally investigated. Functional experiments identified that overexpression of miR-30a increased apoptosis and suppressed cell proliferation, cell migration and cell invasion by directly targeting ZEB2. Collectively, the present study suggested that miR-30a may serve an important role in the progression of NPC and may represent a novel target for the treatment of patients with NPC.

Purpose: The present study set out to investigate the effect of miR-195-5p on cardiomyocyte apoptosis in rats with heart failure (HF) and its mechanism. Methods: HF rat model and hypoxia/reoxygenation (H/R) cardiomyocyte model were established. miR-195-5p expression and transforming growth factor-β1 (TGF-β1)/signal transduction protein (Smad)3 signaling pathway in HF rats and H/R cardiomyocytes were interfered. miR-195-5p expression was tested by Rt-PCR, TGF-β1/Smad3 signaling pathway related proteins were detected by Western Blot, apoptosis of HF rat cardiomyocytes was tested by TUNEL, and apoptosis of cardiomyocytes induced by H/R was checked by flow cytometry. Results: miR-195-5p was lowly expressed in myocardium of HF rats, while TGF-β1 and Smad3 proteins were high-expressed. Up-regulating miR-195-5p expression could obviously inhibit cardiomyocyte apoptosis of HF rats, improve their cardiac function, and inhibit activation of TGF-β1/Smad3 signaling pathway. Up-regulation of miR-195-5p expression or inhibition of TGF-β1/Smad3 signaling pathway could obviously inhibit H/R-induced cardiomyocyte apoptosis. Dual-luciferase reporter enzyme verified the targeted relationship between miR-195-5p and Smad3. Conclusion: miR-195-5p can inhibit cardiomyocyte apoptosis and improve cardiac function in HF rats by regulating TGF-β1/Smad3 signaling pathway, which may be a potential target for HF therapy.