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微管蛋白酪氨酸连接酶类似物12和硝基化酪氨酸对前列腺癌细胞生长的影响
李雅冬1,张劲松1,杨凯1,张福军1,陈睿1,洪苏玲2*
0
(1.重庆医科大学附属第一医院颌面外科,重庆 400016
2.重庆医科大学附属第一医院耳鼻喉头颈外科,重庆 400016
*通信作者)
摘要:
目的 研究微管蛋白酪氨酸连接酶类似物12(TTLL12)和硝基化酪氨酸对前列腺癌细胞生长的影响。方法 利用正常前列腺上皮细胞株PWR1E、RWPE1和前列腺癌细胞株DU145,通过蛋白质印迹分析检测TTLL12和硝基化酪氨酸微管蛋白的表达量,用MTT实验检测细胞的增殖情况。结果 在硝基化酪氨酸的作用下,DU145细胞的硝基化酪氨酸微管蛋白表达量低于PWR1E和RWPE1细胞(P<0.05)。和对照组(以含800 μmol/L盐酸培养)相比,实验组(以含800 μmol/L硝基化酪氨酸的培养液培养)PWR1E和RWPE1细胞增殖受到抑制(P<0.05),而DU145细胞无明显改变(P>0.05)。在有效沉默TTLL12后,实验组(用siTTLL-12转染)的硝基化酪氨酸微管蛋白表达量高于对照组(用siControl转染,P<0.05);实验组内,硝基化酪氨酸使DU145细胞增殖受到抑制(P<0.05),而对照组内,硝基化酪氨酸对细胞增殖改变较小(P>0.05)。结论 TTLL12可使前列腺癌细胞逃避硝基化酪氨酸的打击,从而使前列腺癌细胞逃脱机体监控作用,获得异常增殖机会。
关键词:  微管蛋白酪氨酸连接酶类似物12  硝基化酪氨酸  前列腺肿瘤
DOI:10.3724/SP.J.1008.2012.01
投稿时间:2011-10-23修订日期:2011-11-25
基金项目:重庆市卫生局医学科研计划项目(2011-2-013).
Effect of tubulin tyrosine ligase like 12 and nitrotyrosine on growth of prostate cancer cells
LI Ya-dong1,ZHANG Jin-song1,YANG Kai1,ZHANG Fu-jun1,CHEN Rui1,HONG Su-ling2*
(1. Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016,China
2. Department of Otolaryngology Head and Neck Surgery, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016,China
*Corresponding author.)
Abstract:
Objective To study the effect of tubulin tyrosine ligase like 12 (TTLL12) and nitrotyrosine on the growth of prostate cancer cells. MethodsTTLL12 and α-tubulin nitrotyrosination (N-tubulin) were detected by Western blotting analysis in normal prostate epithelial cell lines PWR1E and RWPE1, and prostate cancer cell line DU145; the proliferation of cells was observed by MTT assay. ResultsThe expression of N-tubulin was significantly lower in DU145 cells than those in PWR1E and RWPE1 cells after treatment with nitrotyrosine (P<0.05). The proliferation of PWR1E and RWPE1 cells treated with nitrotyrosine (cultured with 800 μmol/L nitrotyrosine) were significantly inhibited compared with the control (cultured with 800 μmol/L hydrochloric acid, P<0.05), while there was no visible change in the proliferation of DU145 cells. N-tubulin level was significantly higher in the experimental group (transfected with siTTLL-12) than the control group (transfected with siControl) after effective silence of TTLL12 (P<0.05); the proliferation of DU145 cells treated with nitrotyrosine in the experimental group was significantly inhibited (P<0.05),while there was no visible change in cell proliferation in the control group (P>0.05). ConclusionTTLL12 allows an escape of prostate cancer cells from the treatment of nitrotyrosine,leading to the escape of prostate cancer cells from the body’s surveillance system and acquirement of their abnormal proliferation.
Key words:  tubulin tyrosine ligase like 12  nitrotyrosine  prostatic neoplasms