Long noncoding RNAs have been reported to be important regulators in numerous cancers. In this study, we found that HOXC13 antisense RNA (HOXC13‐AS) was highly expressed in head and neck squamous carcinoma (HNSC) tissues in The Cancer Genome Atlas database. Nasopharyngeal carcinoma (NPC) belongs to HNSC. Therefore, we further investigated the potential role of HOXC13‐AS in NPC. Quantitative reverse transcription polymerase chain reaction examination revealed that HOXC13‐AS was markedly upregulated in NPC tissues and cell lines. Furthermore, HOXC13‐AS was identified as an independent prognosis factor by Cox regression analyses. Subsequently, functional assay revealed that knockdown of HOXC13‐AS impaired cell proliferation, migration, and invasion. Mechanistically, RIP and luciferase reporter analysis confirmed that miR‐383‐3p was a target of HOXC13‐AS. Besides, high mobility group AT‐hook 2 (HMGA2) was proved to be a target of miR‐383‐3p in NPC. Finally, rescue assays demonstrated that HOXC13‐AS functioned as a competing endogenous RNAs to enhance the expression of HMGA2 via sponging miR‐383‐3p. This study suggested that HOXC13‐AS exerted oncogenic function in NPC via regulating miR‐383‐3p/HMGA2 axis, indicating HOXC13‐AS may be a potential therapeutic target for patients with NPC.

2018) Loss of miR-16 contributes to tumor progression by activation of tousled-like kinase 1 in oral squamous cell carcinoma, Cell Cycle, 17:18, 2284-2295, ABSTRACT A different expression signature of miRNA in oral squamous cell carcinoma (OSCC) has been validated. as one of the distinctly dysregulated miRNAs in OSCC, its functional role in progression of OSCC remains not fully clear. Herein, miR-16 expression was significantly lower in OSCC tissues compared to that in adjacent normal tissues (n = 131). A lower level of miR-16 was found to be associated with poor prognosis on a cohort of 131 patients with OSCC, and on an extensive public data (457) from TCGA database. Additionally, expression of TLK1 was significantly higher in OSCC tissues compared to that in adjacent normal tissues, which is negatively correlated with miR-16 expression in OSCC. Bioinformatics analyses exhibited that TLK1 is a potential downstream effector of miR-16 by directly targeting the 3′-untranslated regions (3′-UTR) of mRNA. Forced expression of miR-16 in OSCC cell lines inhibits cell proliferation in vitro, and tumor growth in vivo by inhibition of TLK1. Mechanistically, downregulation of TLK1 by miR-16 enhances higher level of DNA damage leading to a significant increase of G 2 /M arrest in SCC9 cells. And, overexpression of TLK1 substantially reduces DNA damage and G 2 /M arrest by activation of TLK1-dependent cell cycle checkpoint response. To conclude, miR-16 is downregulated in OSCC and serves as tumor suppressor in OSCC progression by targeting TLK1, which has potential to be the novel therapeutic targets and diagnostic biomarkers for OSCC. ARTICLE HISTORY

Six patients presented with recurrent neck abscess, two presented with acute suppurative thyroiditis. All patients had barium swallow and sinus tract was delineated in six cases. All eight patients underwent surgical excision of the sinus tract. Three different emerging pathways of the sinus tract were identified during surgery. The tract could penetrate the thyroid cartilage near the inferior horn, the inferior pharyngeal constrictor muscle or the cricothyroid membrane when it emerged from the larynx. The recurrent laryngeal nerve was commonly dissected to avoid inadvertent damage. Hemithyroidectomy was performed in six patients. All eight are currently asymptomatic.

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Hypopharyngeal squamous cell carcinoma is a common type of malignant tumor among head and neck squamous cell carcinomas (HNSCCs). Heavy smoking and/or drinking is associated with the development of HNSCC. However, HNSCC also occurs in individuals that do not drink or smoke, possibly due to infection with the human papilloma virus (HPV). HPV-16 has been shown to be closely associated with the occurrence of several types of cancers. However, its role in hypopharyngeal squamous cell carcinoma remains unclear. In the present study, we investigated the effects of HPV-16 on hypopharyngeal squamous cell carcinoma and FaDu cells. Lentiviral vectors were used to establish FaDu cells that expressed the E6 and E7 proteins of HPV-16. We used quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assays and western blotting to detect and determine the levels of expression for E6-E7 mRNAs and proteins. Cell Counting Kit-8 (CCK-8) assays, enzyme-linked immunosorbent assays (ELISA), Transwell assays, and flow cytometry were used to assess the effects of HPV-16 E6-E7 on the proliferation, invasion, metastasis and apoptosis of FaDu cells. Expression of microRNAs was analyzed by qRT-PCR. We found that the expression levels of HPV-16 E6-E7 were increased in FaDu cells transfected with the lentiviral vector compared with that observed in the control cells. In addition, the rates of apoptosis were decreased in the transfected cells, while proliferation was increased. The average numbers of cells penetrating the Matrigel were significantly higher than those for the controls. We detected miR-363 and miR-15a, and their expression levels were significantly increased in the HPV-16-positive patients and in FaDu cells expressing HPV-16 E6-E7. We found that HPV-16 E6-E7 appeared to inhibit apoptosis, and to increase cell proliferation, invasion and metastasis. Furthermore, miR-363 and miR-15a were overexpressed in the hypopharyngeal squamous cell carcinoma samples infected with HPV-16, and in FaDu cells stably expressing HPV-16 E6-E7. These findings may provide a new clue of the mechanisms involved in the pathogenesis of HPV-16-positive hypopharyngeal squamous cell carcinoma.