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A variety of ovarian and adrenal diseases can cause elevated levels of androgens in women. This article retrospectively analyzed clinical data of three female patients diagnosed as hyperandrogenism in Tianjin Medical University General Hospital from July 2016 to January 2017 and explored the causes of female hyperandrogenism from different angles.
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<p><b>OBJECTIVE</b>To investigate the effect of sericin on the proliferation of human gastric cancer MKN45 cells and explore the underlying molecular mechanism.</p><p><b>METHODS</b>MKN45 cells were transfected by LC3 double fluorescent autophagic virus, and the positive cells screened by puromycin were divided into blank group, sericin group and sericin∓3-MA group. After incubation with sericin for 48 h, the cells were examined for proliferation, apoptosis and cell cycle using CCK-8 assay and flow cytometry. Cell autophagy was detected by transmission electron microscopy (TEM) and fluorescent inverted microscope, and the autophagy-related markers including LC3, p62 and Beclin proteins were detected with Western blotting. Nude mice bearing gastric cancer xenograft were treated with normal saline or sericin injections (n=5) and the changes in the tumor volume and weight were measured.</p><p><b>RESULTS</b>Compared with the blank group, MKN45 cells with sericin treatment showed significantly inhibited proliferation both in vitro and in nude mice. Autophagosomes were observed in sericin-treated cells under TEM and fluorescent inverted microscope. Sericin treatment of the cells significantly increased the cell apoptosis (P<0.01), caused obvious cell cycle arrest in G/M phase (P<0.01), up-regulated the expressions of both LC3-2 and Beclin, and down-regulated the expression of p62. The autophagy inhibitor 3-MA obviously antagonized the effects of sericin on cell apoptosis, cell cycle and autophagic protein expressions.</p><p><b>CONCLUSION</b>Sericin can inhibit the proliferation of human gastric cancer MKN45 cells by regulating cell autophagy to serve as potential anti-tumor agent.</p>
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<p><b>OBJECTIVE</b>To construct a MYH9 gene knockout model in MGC803 cell line using transcription activator-like effector nuclease (TALEN) and observe its effect on cell cycle and apoptosis.</p><p><b>METHODS</b>According to FastTALE(TM) TALEN Kit, we designed TALEN pairs and constructed the plasmids targeting to MYH9 gene. After detecting their activity in MGC803 cells by plasmid transfection, DNA sequencing, RT-PCR and western blot, we selected the monoclonal cells and studied the changes in the cell cycle and apoptosis.</p><p><b>RESULTS</b>MYH9 gene could not be knocked out but knocked down in selected MGC803 monoclonal cells, which caused cell cycle arrested at G2/M phase (P<0.05) and a significant increase in the cell number with early apoptosis (P<0.01).</p><p><b>CONCLUSION</b>We successfully generated a MYH9 knockdown model in MGC803 cell lines by TALEN, which could be in favor of MYH9 function study in gastric cancer.</p>