...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Animal Cells and Systems >CKS1B promotes the progression of hepatocellular carcinoma by activating JAK/STAT3 signal pathway
【24h】

CKS1B promotes the progression of hepatocellular carcinoma by activating JAK/STAT3 signal pathway

机译：CKS1B通过激活Jak / Stat3信号途径促进肝细胞癌的进展

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Hepatocellular carcinoma (HCC) is a malignancy of considerable concern due to its continuous increase in morbidity and mortality. This study attempts to identify the molecules that play a key role in the progression of HCC, explore its potential mechanism, and provide more target choices for targeted therapy. Using overexpression plasmid and shRNA, CKS1B was respectively overexpressed and knocked down to explore its biological function roles in HCC progression and development. MTT and colony formation assays showed that knockdown of CKS1B inhibited the survival and proliferation of HCC cell lines (Hep3B and Huh7). The flow cytometry and western blot analysis showed that knockdown of CKS1B significantly induced the apoptosis of Hep3B and Huh7 cells. The wound healing and transwell invasion assays showed that knockdown of CKS1B had a significant inhibitory effect on the migration and invasion of Hep3B and Huh7 cells. These functional tests confirmed that CKS1B acts as an oncogene that regulates the malignant progression of HCC. Moreover, this study also demonstrated that knockdown of CKS1B inhibited the activation of JAK/STAT3 pathway, evidenced by the significantly downregulated p-STAT3 protein expression. Furthermore, knockdown of CKS1B also downregulated STAT3 target genes TIMP-1, Bcl-2 and VEGF, which were involved in controlling cell apoptosis and migration. On the contrary, overexpression of CKS1B caused the completely opposite results. Taken together, CKS1B acts as an oncogene to promote the proliferation and metastasis of HCC cells by activating JAK/STAT3 signaling pathway.
机译：肝细胞癌（HCC）是由于其持续增加了发病率和死亡率，这是一个显着关注的恶性肿瘤。本研究试图识别在HCC进展中发挥关键作用的分子，探讨其潜在机制，并为有针对性治疗提供更多的目标选择。使用过表达质粒和shRNA，CKS1b分别过表达并敲下来，以探讨其在HCC进展和发育中的生物功能作用。 MTT和菌落形成测定显示CKS1B的敲低抑制HCC细胞系（HEP3B和HUH7）的存活率和增殖。流式细胞术和Western印迹分析表明，CKS1B的敲低显着诱导了HEP3B和HUH7细胞的凋亡。伤口愈合和Transwell入侵测定显示CKS1B的敲低对HEP3B和HUH7细胞的迁移和侵袭具有显着的抑制作用。这些功能性测试证实，CKS1B作为调节HCC恶性进展的癌基因。此外，该研究还证明了CKS1B的敲低抑制了JAK / Stat3途径的激活，通过显着下调的P-Stat3蛋白表达证明。此外，CKS1B的敲低也下调了STAT3靶基因TIMP-1，BCL-2和VEGF，其参与控制细胞凋亡和迁移。相反，CKS1B的过度表达导致完全相反的结果。 CLES1B携带，作为癌基因，通过激活JAK / Stat3信号通路来促进HCC细胞的增殖和转移。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号