[The clinical characteristics and treatment strategies of differentiated thyroid carcinoma in adolescents and children].

Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi

Department of Otolaryngology Head and Neck Surgery, the First Hospital of Shanxi Medical University, Shanxi Key Laboratory of Otorhinolaryngology Head and Neck Cancer, Key Institute and Laboratory of Otolaryngology Affiliated with Shanxi Province,Taiyuan,030001,China.

Published: April 2017

To investigate the effects of hsa-miR-193b on the proliferation and apoptosis of Hep-2 cells.The experiment was divided into Blank, NC, and miR-193b inhibitor. We used the qRT-PCR to identify the expression of miR-193b in Hep-2 cells. Cell proliferation was monitored using the MTT assay kit. Cell cycle and apoptosis were analyzed by flow cytometry. Cell invasion was monitored using the Transwell assay staining. The target of miR-193b was forecasted by bioinformatics.The expression level of SMAD3 protein was detected by Western blot. After miR-193b inhibitor transfection, qRT-PCR showed that the expression of miR-193b was downregulated significantly (compared with Blank and NC,<0.01),and there was no significant difference between Blank and NC(>0.05). Compared with NC, miR-193b inhibitor induced a significant inhibition of cells growth at 24 h, 48 h and 72 h(<0.05,<0.01 and <0.01), and flow cytometry revealed that miR-193b inhibitor significantly promoted cell apoptosis(<0.01) and cell cycle was blocked in G1/S stage(<0.01), meanwhile miR-193b inhibitor also inhibited the invasive property of Hep-2 cells(<0.01). Predicting outcomes indicated that SMAD3 was a target of miR-193b. Furthermore, the over-expression of miR-193b down-regulated the expression of SMAD3(compared with NC,<0.05). miR-193b inhibitor can inhibit the proliferation, migration and invasion abilities, and promote the apoptosis of Hep-2 cells. It indicates that miR-193b acts as an "oncogene" for laryngal squamous cell carcinoma and may serve as a novel antitumor target of therapy.

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http://dx.doi.org/10.13201/j.issn.1001-1781.2017.07.006DOI Listing

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