PDF(Pubmed)
Abstract：
UNASSIGNED: Inhibitor of NF-κB kinase-interacting protein (IKIP) is known to promote proliferation of glioblastoma (GBM) cells, but how it affects migration and invasion by those cells is unclear.
UNASSIGNED: We compared levels of IKIP between glioma tissues and normal brain tissue in clinical samples and public databases. We examined the effects of IKIP overexpression and knockdown on the migration and invasion of GBM using transwell and wound healing assays, and we compared the transcriptomes under these different conditions to identify the molecular mechanisms involved.
UNASSIGNED: Based on data from our clinical samples and from public databases, IKIP was overexpressed in GBM tumors, and its expression level correlated inversely with survival. IKIP overexpression in GBM cells inhibited migration and invasion in transwell and wound healing assays, whereas IKIP knockdown exerted the opposite effects. IKIP overexpression in GBM cells that were injected into mouse brain promoted tumor growth but inhibited tumor invasion of surrounding tissue. The effects of IKIP were associated with downregulation of THBS1 mRNA and concomitant inhibition of THBS1/FAK signaling.
UNASSIGNED: IKIP inhibits THBS1/FAK signaling to suppress migration and invasion of GBM cells.
UNASSIGNED: We compared levels of IKIP between glioma tissues and normal brain tissue in clinical samples and public databases. We examined the effects of IKIP overexpression and knockdown on the migration and invasion of GBM using transwell and wound healing assays, and we compared the transcriptomes under these different conditions to identify the molecular mechanisms involved.
UNASSIGNED: Based on data from our clinical samples and from public databases, IKIP was overexpressed in GBM tumors, and its expression level correlated inversely with survival. IKIP overexpression in GBM cells inhibited migration and invasion in transwell and wound healing assays, whereas IKIP knockdown exerted the opposite effects. IKIP overexpression in GBM cells that were injected into mouse brain promoted tumor growth but inhibited tumor invasion of surrounding tissue. The effects of IKIP were associated with downregulation of THBS1 mRNA and concomitant inhibition of THBS1/FAK signaling.
UNASSIGNED: IKIP inhibits THBS1/FAK signaling to suppress migration and invasion of GBM cells.
摘要：
■已知NF-κB激酶相互作用蛋白（IKIP）的抑制剂可促进胶质母细胞瘤（GBM）细胞的增殖，但它如何影响这些细胞的迁移和入侵尚不清楚。
■我们在临床样本和公共数据库中比较了神经胶质瘤组织和正常脑组织之间的IKIP水平。我们使用transwell和伤口愈合试验检查了IKIP过表达和敲低对GBM迁移和侵袭的影响。我们比较了这些不同条件下的转录组，以确定所涉及的分子机制。
■根据我们的临床样本和公共数据库的数据，IKIP在GBM肿瘤中过度表达，其表达水平与生存率呈负相关。GBM细胞中IKIP过表达抑制了transwell和伤口愈合试验中的迁移和侵袭,而IKIP敲除产生相反的效果。注射到小鼠脑中的GBM细胞中的IKIP过表达促进了肿瘤生长，但抑制了肿瘤对周围组织的侵袭。IKIP的作用与THBS1mRNA的下调和伴随的THBS1/FAK信号传导的抑制有关。
■IKIP抑制THBS1/FAK信号传导以抑制GBM细胞的迁移和侵袭。
■我们在临床样本和公共数据库中比较了神经胶质瘤组织和正常脑组织之间的IKIP水平。我们使用transwell和伤口愈合试验检查了IKIP过表达和敲低对GBM迁移和侵袭的影响。我们比较了这些不同条件下的转录组，以确定所涉及的分子机制。
■根据我们的临床样本和公共数据库的数据，IKIP在GBM肿瘤中过度表达，其表达水平与生存率呈负相关。GBM细胞中IKIP过表达抑制了transwell和伤口愈合试验中的迁移和侵袭,而IKIP敲除产生相反的效果。注射到小鼠脑中的GBM细胞中的IKIP过表达促进了肿瘤生长，但抑制了肿瘤对周围组织的侵袭。IKIP的作用与THBS1mRNA的下调和伴随的THBS1/FAK信号传导的抑制有关。
■IKIP抑制THBS1/FAK信号传导以抑制GBM细胞的迁移和侵袭。
