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Long noncoding RNAs (lncRNAs) are associated with the development, progression, and prognosis of human cancers. However, the clinical significance and biological function of lncRNAs in hypopharyngeal squamous cell carcinoma (HSCC) remain largely unknown. We characterized the novel lncRNA AB209630 in vivo and in vitro. First, using qRT-PCR, we evaluated whether AB209630 levels differ between HSCC tissues/cell lines and adjacent normal tissues/cell lines. We then assessed whether AB209630 expression levels stimulate or inhibit proliferation, invasion, apoptosis, and metastasis in vitro. Finally, we investigated whether AB209630 levels in tumor tissues were associated with survival outcomes. Our results demonstrated that AB209630 levels were markedly lower in HSCC tissues and cells than in normal tissues and cells, and increased expression of AB209630 level significantly inhibited growth, metastasis, and invasion and stimulated apoptosis in vitro. In addition, patients with decreased expression of AB209630 had a significantly poorer prognosis than those with high AB209630 expression. These data suggest that increased expression of AB209630 might either stimulate or inhibit biological activities involved in HSCC development, indicating a potential application of AB209630 in future treatment for this disease. This study suggest that AB209630 functions as a tumor suppressor in HSCC, and its decreased expression may help predict a poor prognostic outcome of HSCC. Our future work will focus on the mechanisms of whether and how AB209630 as a tumor suppressor gene is involved in HSCC development.

MicroRNAs (miRNAs) are aberrantly expressed in several tumors and play important role in tumorigenesis. However, little is known about the role of miR-613 in laryngeal squamous cell carcinoma (LSCC). We determined the expression of miR-613 in a panel of 30 LSCC specimens. Compared with the adjacent normal samples, 20 cases of LSCC tissues exhibited decreased expression of miR-613. The average expression of miR-613 in LSCC tissues was lower than in normal samples. Moreover, we demonstrated that exogenous expression of miR-613 suppressed LSCC cell proliferation, invasion, and blocked G1/S phase transition. We identified that 3-phosphoinositide-dependent protein kinase-1 (PDK1) was a direct target gene of miR-613 in LSCC cell. Overexpression of miR-613 suppressed PDK1 expression in LSCC cell. Furthermore, we demonstrated that PDK1 was upregulated in LSCC tissues. MiR-613 expression was inversely correlated with the expression of PDK1 in LSCC tissues. Moreover, we showed that PDK1 was involved in the miR-613-mediated cancer suppression of LSCC cell. These results suggested that miR-613 played as a tumor suppressor gene in LSCC partly by inhibiting PDK1 expression.