[1]陈海平,向玘,刘大伟,等.沉默CIT基因可抑制前列腺癌细胞的增殖和转移[J].南方医科大学学报,2019,(03):257.[doi:10.12122/j.issn.1673-4254.2019.03.01]
点击复制

沉默CIT基因可抑制前列腺癌细胞的增殖和转移()
分享到:

《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2019年03期
页码:
257
栏目:
出版日期:
2019-04-11

文章信息/Info

Title:
Citron Rho-interacting serine/threonine kinase knockdown suppresses prostate cancer cell proliferation and metastasis by blocking Hippo-YAPpathway
作者:
陈海平向玘刘大伟魏强
关键词:
丝/苏氨酸激酶前列腺癌转移上皮-间质转化Hippo-YAP通路
Keywords:
Citron Rho-interacting serine/threonine kinase prostate cancer invasion migration Hippo-YAPpathway
DOI:
10.12122/j.issn.1673-4254.2019.03.01
摘要:
目的探究Citron Rho-interacting serine/threonine kinase(CIT)基因在前列腺癌中的表达特点,并探讨CIT基因对PC-3细 胞增殖、迁移和侵袭能力的调控作用及其可能的分子机制。方法利用TCGA和MSKCC数据库分析CIT在前列腺癌组织的表 达水平和临床相关性。采用siRNA干扰CIT的表达,采用CCK-8、划痕实验和Transwell实验检测CIT对前列腺癌PC-3细胞系 的增殖、迁移和侵袭特性的影响。采用Western blotting检测CIT对上皮-间质转化和Hippo-YAP通路的调控作用。结果TCGA 数据库分析表明,CIT在前列腺癌组织中表达显著上调(P<0.05);MSKCC数据库分析表明,CIT表达水平与N分期(P<0.05)、M 分期(P<0.001)、Gleason评分(P=0.010)和PSA水平(P=0.004)成正相关关系。PC-3细胞中沉默CIT表达可显著抑制细胞的增 殖、迁移和侵袭,逆转上皮-间质转化进程,并抑制Hippo-YAP通路的激活。结论CIT基因可能是前列腺癌的致病基因,其分子 机制可能与Hippo-YAP通路的激活有关。
Abstract:
Objective Citron Rho-interacting serine/threonine kinase (CIT) was identified recently as an oncogene involved in the progression of various malignant tumors, but its role in prostate cancer (PCa) remains unclear. In this study,we aimed to investigate the biological functions of CIT in PCa. MethodsWe analyzed the expression of CIT in PCa tissues and its clinical correlations based on the Cancer Genome Atlas (TCGA) and Memorial Sloan-Kettering Cancer Center (MSKCC) dataset.We then examined the effects of RNA interference-mediated CIT silencing on the proliferation, migration and invasion of PC-3 cells using cell counting kit-8, wound healing assay and Transwell assay. We also investigated the effect of CIT silencing on epithelial-mesenchymal transition (EMT) and Hippo-Yap signaling pathway in the cells using Western blotting. Results CIT expression was significantly elevated in PCa tissues from TCGA cohort (P<0.05). MSKCC dataset analysis showed that an elevated expression of CIT was significantly correlated with N stage (P=0.001), distant metastasis (P<0.001), Gleason score (P=0.010) and PSA (P=0.004). In cultured PC-3 cells, knockdown of CIT significantly inhibited cell proliferation, migration and invasion, reversed the EMT phenotype and decreased the expression and activity of YAP. Conclusion CIT might function as an oncogene in PCa by modulating the Hippo-YAP signaling pathway and serve as a candidate therapeutic target for PCa.

相似文献/References:

[1]邓凡 王春霞 许万福 冯丽 柯志勇 Wang Q. Jane 邹志鹏. PKD3上调前列腺癌细胞中PSA表达及机制[J].南方医科大学学报,2010,(08):1779.
 DENG Fan,WANG Chun-xia,XU Wan-fu,et al. PKD3 contributes to up-regulation of prostate-specific antigen in prostate cancer cells[J].Journal of Southern Medical University,2010,(03):1779.
[2]荆玉明,罗杰,张艳玲,等.p38丝裂原激活蛋白激酶基因重组慢病毒载体的构建及其在建立人前列腺癌稳定细胞株中的应用[J].南方医科大学学报,2012,(03):317.
[3]董金凯,罗津,阎瑾琦,等.小鼠前列腺干细胞抗原的原核表达、纯化及抗原活性检测[J].南方医科大学学报,2012,(04):502.
[4]李炬聪,宋先璐,陆斌,等.晚期糖基化终末产物受体胞外段不同功能段在前列腺癌细胞中的表达与定位[J].南方医科大学学报,2012,(04):507.
[5]王威,高江平,徐阿祥,等.腹膜外途径机器人辅助腹腔镜根治性前列腺切除术:附20例报告[J].南方医科大学学报,2012,(05):749.
[6]崔明星,詹新立,刘会江,等.人前列腺癌PC-3细胞的荧光标记及其脊椎转移动物模型的建立[J].南方医科大学学报,2013,(02):243.
[7]刘欣,王节,张舜欣,等.北京地区临床无前列腺癌人群年龄相关性前列腺特异性抗原的参考范围[J].南方医科大学学报,2013,(11):1704.
[8]傅伟,彭辉,陈志强,等.罕见肺腺癌前列腺转移1例报告并文献复习[J].南方医科大学学报,2014,(02):289.
[9]王一茹,姚斌伟,张艳,等.FoxM1 shRNA慢病毒载体构建及感染人前列腺癌细胞的稳定细胞株筛选[J].南方医科大学学报,2015,(09):1227.
[10]徐亚文,陈玢屾,许凯,等.RNA干扰IgG表达对人前列腺癌细胞株PC3放射敏感性的影响[J].南方医科大学学报,2015,(03):397.

更新日期/Last Update: 1900-01-01