The study evaluated the ability of long intergenic noncoding RNA LINC00312 (LINC00312) to influence the proliferation, invasion, and migration of thyroid cancer (TC) cells by regulating miRNA-197-3p. TC tissues and adjacent normal tissues were collected from 211 TC patients. K1 (papillary TC), SW579 (squamous TC), and 8505C (anaplastic TC) cell lines were assigned into a blank, negative control (NC), LINC00312 overexpression, miR-197-3p inhibitors, and LINC00312 overexpression + miR-197-3p mimics group. The expression of LINC00312, miR-197-3p, and p120 were measured using quantitative real-time PCR (qRT-PCR) and Western blotting. Cell proliferation was assessed via CCK8 assay, cell invasion through the scratch test, and cell migration via Transwell assay. In comparison with adjacent normal tissues, the expression of LINC00312 is down-regulated and the expression of miR-197-3p is up-regulated in TC tissues. The dual luciferase reporter gene assay confirmed that P120 is a target of miR-197-3p. The expression of LINC00312 and p120 was higher in the LINC00312 overexpression group than in the blank and NV groups. However, the expression of miR-197-3p was lower in the LINC00312 overexpression group than in the blank and NC groups. The miR-197-3p inhibitors group had a higher expression of miR-197-3p, but a lower expression of p120 than the blank and NC groups. The LINC00312 overexpression and miR-197-3p inhibitor groups had reduced cell proliferation, invasion and migration than the blank and NC groups. These results indicate that a LINC00312 overexpression inhibits the proliferation, invasion, and migration of TC cells and that this can be achieved by down-regulating miR-197-3p.

Background The pathogenesis of chronic rhinosinusitis (CRS) is not yet clear. microRNAs are widely involved in a number of physiological and pathological processes, of which microRNA-146a (miR-146a) plays an important role in innate immunity, inflammatory response, and other pathophysiological processes. Mucins (MUCs) are important components of secreted mucus, of which MUC5AC is the major MUC secreted in the normal airway. Objective This study was performed to examine human neutrophil elastase (HNE)-induced MUC5AC overexpression in CRS via miR-146a. Methods miR-146a, HNE, epidermal growth factor receptor (EGFR), and MUC5AC expression in the sinonasal mucosa were determined using quantitative real-time polymerase chain reaction (qRT-PCR). EGFR, phosphorylated EGFR (pEGFR), and MUC5AC expression were determined in primary cultures of human nasal epithelial cells (HNECs). We examined the expression of miR-146a, MUC5AC, EGFR, and pEGFR by transfecting HNECs with miR-146a mimics and negative control (NC). Moreover, dual-luciferase reporter gene assays were used to validate EGFR as an hsa-miR-146a target gene. Results miR-146a was significantly downregulated, and HNE, EGFR, and MUC5AC were upregulated in CRS patients both with and without nasal polyps. In the in vitro cell experiment, MUC5AC was significantly downregulated after use of an EGFR-specific inhibitor (AG1478). Upon addition of miR-146a inhibitor, miR-146a was downregulated, while MUC5AC was upregulated. MUC5AC was suppressed in normal primary HNECs by miR-146a mimic and pEGFR was downregulated. The results of dual-luciferase reporter assays showed that the luciferase activities were markedly inhibited in the pGL3-EGFR-3′ UTR+miR-146a mimic group compared with the pGL3+ miR-146a mimic group, suggesting that EGFR is a target gene for miR-146a. Conclusion In HNE-induced CRS, miR-146a downregulates the expression of MUC5AC by inhibiting the activation of EGFR, and EGFR is a target gene of miR-146a.

Background Hypersecretion of mucin 5AC (MUC5AC) is a prominent feature of chronic rhinosinusitis with nasal polyps (CRSwNP) and autophagy plays a pivotal role in this process. TNF receptor-associated factor 6 (TRAF6) functions as a signal transducer in many inflammation diseases, whereas the correlation between TRAF6 and autophagy in CRSwNP remains unclear. Objective To investigate the role of TRAF6 in the human neutrophil elastase (HNE)-induced autophagy and mucin MUC5AC over-expression in CRSwNP. Methods Tissue specimens were obtained from control subjects and patients with CRSwNP. The relationships between HNE, TRAF6, autophagy, and MUC5AC were investigated. The effect of TRAF6 on HNE-mediated autophagy and hypersecretion of MUC5AC was assessed by in-vitro culture of HNECs treated with human recombinant HNE. Results Patients with CRSwNP had more protein expression of HNE, MUC5AC, TRAF6, and light chain (LC3B), and increased levels of Beclin-1(BECN1) and autophagy-related gene 5 (ATG5) in mRNA level. Treatment of nasal epithelial cells with recombinant HNE induced the upregulation of TRAF6, autophagy, and MUC5AC. Alternatively, si-TRAF6 or autophagy inhibitor treatment mitigates the hyperexpression of MUC5AC before incubating with recombinant HNE. Conclusion HNE promotes autophagy through TRAF6, resulting in hyperexpression of MUC5AC in CRSwNP.

The laryngopharyngeal reconstruction in patients with pyriform sinus carcinoma continues to be a challenge for surgeons. In this article, we describe our experience with laryngopharyngeal reconstruction in patients with pyriform sinus carcinoma using the modified infrahyoid myocutaneous flap (IHMCF). The modified incision design for the modified IHMCF and clinical outcomes are also detailed here. Between January 2012 and February 2018, 10 patients with hypopharyngeal squamous cell carcinoma who underwent laryngopharyngeal reconstruction using the modified IHMCF after hemicricolaryngopharyngectomy were included in this study. The drainage vessels of the modified IHMCF, oncological outcomes, and functional reservation of the larynx were recorded. All of the flaps survived well. No flap necrosis or other major complications occurred during follow-up. None of the patients remained on nasogastric feeding for more than 4 weeks postoperatively. The follow-up period ranged from 12 to 73 months (mean, 36 months). In our series, 6 patients were successfully decannulated and 5 had received radiation therapy. We roughly assessed the speech and swallowing functions, and the outcomes seemed acceptable in all of the patients after surgery. Laryngoscopic examination showed that the modified IHMCF survived well and the new glottis provided excellent function and good ventilation results. In our experience, the modified IHMCF is a safe and viable procedure that can serve as a valid alternative to free flaps and the pectoralis major myocutaneous flap to reconstruct laryngopharyngeal defects.

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