Zhang H

Overexpression of TP53 mutation-associated microRNA-182 promotes tumor cell proliferation and migration in head and neck squamous cell carcinoma

OBJECTIVE To investigate the functional mechanism of microRNA-182 (miR-182) in head and neck squamous cell carcinoma (HNSCC). DESIGN HNSCC and normal samples were used to check both p53 and miR-182 expression. Two cancer cell lines with overexpression of miR-182 were used to check cell proliferation and migration. In vivo role of miR-182 was assessed using mouse xenograft tumor model. β-TrCP2 was found to be direct target of miR-182 by luciferase reporter assay. RESULTS Overexpression of miR-182 was closely related with overproduction of p53 in HNSCC. Overexpression of miR-182 promoted cell proliferation and migration and its oncogenic effect was also confirmed in vivo. β-TrCP2 acted as direct target of miR-182 and its overexpression can reverse the miR-182 induced cell proliferation and migration. CONCLUSION Overexpression of TP53 mutation-associated miR-182 may promote tumor cell proliferation and migration in HNSCC and suggest possible biomarker for the prediction of tumor recurrence.

Preliminary proteomic analysis of human serum from patients with laryngeal carcinoma.

To better evaluate the serum protein alterations in patients with laryngeal carcinoma during surgical treatment process, a comparative proteomic analysis of human serum from patients with laryngeal carcinoma between pre- and post-operation group was performed using two-dimensional gel electrophoresis, in combination with matrix-assisted laser desorption ionization time-of-flight mass spectrometry and database searching. Statistical analysis indicated that 16 gel spots corresponding to 12 proteins altered their expression significantly between the two groups of patients with laryngeal carcinoma. Of these 12 proteins, 6 proteins were up-regulated in the pre-operation group. The subsequent Western blot confirmed the results of proteome analysis. Measurement of MDA and SOD levels in serum combining with bioinformatics analysis indicated the potential roles of the oxidant stress and immune response as target in monitoring and treating laryngeal carcinoma. The study provides new insight into the laryngeal carcinoma development and treatment, and the identified proteins are warranted to be further studied.

Polysaccharides from Citrus grandis associate with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophages

Chronic pharyngitis is characterized as a common inflammation of the pharyngeal mucosa, and anti-inflammatory medications are the common treatment to relieve it. Polysacharides of Citrus grandis L. Osbeck (PCG) and luteolin have been reported to have anti-inflammatory activities. In this study, the protective effects of PCG and luteolin on chronic pharyngitis are evaluated and the underlying mechanisms are explored. PCG and luteolin are administrated to animal models with granuloma, ear edema and chronic pharyngitis and the effects of PCG and luteolin on disease severity are evaluated. We also evaluate the effects of PCG and luteolin on inflammatory cytokine production in macrophages stimulated with lipopolysaccharides (LPS)/interferon-gamma (IFN-γ) and detect the effects of PCG and luteolin on macrophage polarization. Finally, we evaluate the effects of PCG and luteolin on activations of LPS-induced downstream signaling pathways. PCG and luteolin alleviate the disease severity of granuloma, ear edema and chronic pharyngitis. PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.