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<p><b>OBJECTIVE</b>This study aimed to investigate the ratio of T helper cell 17 (Th17) and regulatory T cells (Treg) in peripheral blood of oral lichen planus (OLP) and explore the pathogenesis of its possible role and significance.</p><p><b>METHODS</b>The peripheral blood samples were obtained from 33 patients with OLP (15 cases of reticular OLP and 18 cases of erosive OLP) and 17 healthy controls. The percentages of Th17 and Treg cells were detected by flow cytometry (FCM). Real-time fluorescence quantitative polymerase chain reaction (qPCR) technique was used to detect the expression levels of retinoid-related orphan nuclear receptor γt (RORγt) and forkhead box 3 (Foxp3).</p><p><b>RESULTS</b>The proportions of Th17, Treg cells, and their transcription factors (RORγt and Foxp3) in OLP were higher than those in the control groups (P<0.05). By contrast, in Treg cells and Foxp3, no significance was observed between erosive OLP and reticular OLP. Th17/Treg ratio increased in OLP. This ratio was significantly increased in erosive OLP compared with those in the control groups and reticular OLP (P<0.01). Nevertheless, no significance was noted between reticular OLP and control groups. Statistical analysis demonstrated positive correlations among Th17 cells, Th17/Treg, and clinical characteristics (r=0.66, P=0.00; r=0.66, P=0.00; r=0.52, P=0.00; r=0.50, P=0.00). Positive correlations also existed between Th17 and Treg cells (r=0.39, P=0.03).</p><p><b>CONCLUSIONS</b>Th17 cells, Treg cells, and their ratios all increased in the peripheral blood of OLP. Moreover, the imbalance inTh17/Treg may play a role in the pathogenesis of erosive OLP.</p>
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PURPOSE: Chloride channel-3 (ClC-3) is a member of the chloride channel family and plays a critical role in a variety of cellular activities. The aim of the present study is to explore the molecular mechanisms underlying the antitumor effect of silencing ClC-3 in breast cancer. METHODS: Human breast cancer cell lines MDA-MB-231 and MCF-7 were used in the experiments. Messenger RNA and protein expression were examined by quantitative real-time polymerase chain reaction and western blot analysis. Cell proliferation was measured by the bromodeoxyuridine method, and the cell cycle was evaluated using fluorescence-activated cell sorting. Protein interaction in cells was analyzed by co-immunoprecipitation. Tumor tissues were stained with hematoxylin-eosin and tumor burden was measured using the Metamorph software. RESULTS: Breast cancer tissues collected from patients showed an increase in ClC-3 expression. Knockdown of ClC-3 inhibited the secretion of insulin-like growth factor (IGF)-1, cell proliferation, and G1/S transition in breast cancer cells. In the mouse xenograft model of human breast carcinoma, tumor growth was significantly slower in animals injected with ClC-3-deficient cells compared with the growth of normal human breast cancer cells. In addition, silencing of ClC-3 attenuated the expression of proliferating cell nuclear antigen, Ki-67, cyclin D1, and cyclin E, as well as the activation of extracellular signal-regulated protein kinases (ERK) 1/2, both in vitro and in vivo. CONCLUSION: Together, our data suggest that upregulation of ClC-3 by IGF-1 contributes to cell proliferation and tumor growth in breast cancer, and ClC-3 deficiency suppresses cell proliferation and tumor growth via the IGF/IGF receptor/ERK pathway.