Kim Yoon Jung, Hwang Hyo-Jeong, Kang Jun Goo, Kim Chul Sik, Ihm Sung-Hee, Choi Moon Gi, Lee Seong Jin
Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Hallym University, Chuncheon, Republic of Korea.
Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Hallym University, Chuncheon, Republic of Korea
Anticancer Res. 2018 Jun;38(6):3515-3525. doi: 10.21873/anticanres.12623.
BACKGROUND/AIM: The aim of the present study was to assess the role of enigma protein in survival of thyroid carcinoma cells.
BCPAP and 8505C human thyroid carcinoma cells were used. Cell viability using CCK-8 assay, the percentage of dead cells using trypan blue assay, cytotoxic activity using cytotoxicity assay, cell growth rate and cell migration using wound-healing assay were performed.
In enigma siRNA-transfected cells, cell viability, and the protein levels of AKT and survivin decreased. The percentage of dead cells, cytotoxic activity and cleaved poly (ADP-ribose) polymerase (PARP) protein levels increased. After transfection of p110α plasmid, the alterations in cell viability, the percentage of dead cells, cytotoxic activity, and protein levels of AKT, survivin and cleaved PARP were abrogated. Cell growth rate and cell migration were reduced with reduction of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) protein levels, as well as increased p53 and p21 protein levels.
Enigma affects cell survival through modulation of phosphatidylinositol-3 kinase/AKT signaling and survivin, and regulates cell proliferation and migration via involvement of MMP-2, MMP-9, p53 and p21 in thyroid carcinoma cells.
背景/目的:本研究旨在评估谜蛋白在甲状腺癌细胞存活中的作用。
使用BCPAP和8505C人甲状腺癌细胞。采用CCK-8法检测细胞活力,台盼蓝法检测死细胞百分比,细胞毒性试验检测细胞毒性活性,伤口愈合试验检测细胞生长速率和细胞迁移。
在转染谜蛋白小干扰RNA的细胞中,细胞活力以及AKT和生存素的蛋白水平降低。死细胞百分比、细胞毒性活性和裂解的聚(ADP-核糖)聚合酶(PARP)蛋白水平升高。转染p110α质粒后,细胞活力、死细胞百分比、细胞毒性活性以及AKT、生存素和裂解PARP的蛋白水平的改变被消除。随着基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶-9(MMP-9)蛋白水平的降低以及p53和p21蛋白水平的升高,细胞生长速率和细胞迁移降低。
谜蛋白通过调节磷脂酰肌醇-3激酶/AKT信号传导和生存素来影响细胞存活,并通过参与甲状腺癌细胞中的MMP-2、MMP-9、p53和p21来调节细胞增殖和迁移。