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Background: Increasing evidence shows that long non-coding RNAs (lncRNAs) play a key role in the development of various cancers. Zinc finger antisense 1 (ZFAS1) is a novel lncRNA with previously demonstrated associations with several types of cancer. Here we examined the expression and potential function of the ZFAS1 in nasopharyngeal carcinoma (NPC)., Methods: We detected ZFAS1 expression in GSE12452, a human microarray dataset, and NPC cell lines. Small interfering RNA against ZFAS1 was used to elucidate the cellular functions of ZFAS1 using MTT, colony formation, cell cycle, cell apoptosis, transwell invasion and migration and western blot assays. An activator of the PI3K/AKT signaling pathway (740Y-P) was used to determine the contribution of PI3K/AKT., Results: ZFAS1 was significantly upregulated in NPC tissues and cell lines. Silencing ZFAS1 significantly inhibited cell proliferation and invasion, arrested cell cycle progression and promoted cell apoptosis, as well as reduced epithelial-mesenchymal transition. Moreover, 740Y-P could rescue the effects of ZFAS1 knockdown on proliferation, apoptosis and invasion in 5-8F cells., Conclusions: ZFAS1 might play an oncogenic role in NPC and facilitate cell proliferation and invasion via the PI3K/AKT signaling pathway in NPC cells.

Background: Circular RNAs (circRNAs) have been shown to play a crucial role in tumorigenesis. In this study, we investigated the function of hsa_circ_0137008 and its underlying molecular mechanism in colorectal cancer (CRC). Methods: Gene expression was conducted by quantitative real-time PCR or western blot. Functional experiments were performed by cell count kit-8, colony formation assay, wound healing, and transwell assays. Luciferase reporter assay and RNA pull-down assay were performed to investigate the molecular mechanism of hsa_circ_0137008 in CRC. In addition, the xenograft tumor model was applied to determine the role of hsa_circ_0137008 in vivo. Results: Downregulation of hsa_circ_0137008 was observed in CRC tissues and cell lines. Functionally, overexpression of hsa_circ_0137008 inhibited the proliferation of CRC cells, as indicated by the inhibition of proliferative protein expression (Ki67 and PCNA), reduced cell viability and colony formation ability. Upregulation of hsa_circ_0137008 suppressed the migration, invasion, and epithelial to mesenchymal transition (EMT) of CRC cells. Mechanically, hsa_circ_0137008 negatively regulated the expression of microRNA-338-5p (miR-338-5p). Furthermore, hsa_circ_0137008 abated the miR-338-5p mediated promotion on CRC cell progression. Tumor suppressive function of hsa_circ_0137008 was validated in vivo. Conclusion: These findings highlighted the fact that overexpression of hsa_circ_0137008 inhibited the progression of CRC via sponging miR-338-5p, suggesting that hsa_circ_0137008/miR-338-5p axis is a principal regulator of CRC tumorigenesis. [ABSTRACT FROM AUTHOR]

Background/Aims: miR-802 plays a key role in cancer progression and development. The purpose of this work is to investigate the functional role of miR-802 in laryngeal cancer and to elucidate the function of miR-802 and cAMP-regulated phosphoprotein 19 (ARPP19) on laryngeal cancer. Methods: RT-qPCR was applied to study the expression level of ARPP19 and miR-802 in the laryngeal carcinoma cell lines and tissues. CCK-8, colony formation, flow cytometry (FACS) assay were used to study the effect of ARPP19 and miR-802 on apoptosis, proliferation, and cell cycle of laryngeal carcinoma cells. Target gene prediction and luciferase reporter gene assay were applied to identify target gene of miR-802. The transcriptional mRNA and protein expression levels of ARPP19 were measured by RT-qPCR or Western blotting. Results: miR-802 was down-regulated in laryngeal carcinoma cell lines and tissues. Laryngeal cancer cells transfected by miR-802 mimic were significantly inhibited in the terms of cell colony formation and proliferation. Furthermore, miR-802 can inhibit the expression level of ARPP19 by directly targeting the 3ʹ untranslated region (3ʹ-UTR) of ARPP19. Overexpression of the ARPP19 gene can reverse the suppressive effect of miR-802 on laryngeal cancer cells. Conclusion: miR-802 can exert tumor suppressor effects in laryngeal carcinoma by targeting ARPP19, indicating that miR-802 protein may play a role of potential therapeutic target for clinical laryngeal cancer. [ABSTRACT FROM AUTHOR]