{"title":"IKIP 可下调 THBS1/FAK 信号，从而抑制胶质母细胞瘤细胞的迁移和侵袭。","authors":"Zhaoying Zhu, Yanjia Hu, Feng Ye, Haibo Teng, Guoliang You, Yunhui Zeng, Meng Tian, Jianguo Xu, Jin Li, Zhiyong Liu, Hao Liu, Niandong Zheng","doi":"10.32604/or.2024.042456","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>IKIP inhibits THBS1/FAK signaling to suppress migration and invasion of GBM cells.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"32 7","pages":"1173-1184"},"PeriodicalIF":2.0000,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11211642/pdf/","citationCount":"0","resultStr":"{\"title\":\"IKIP downregulates THBS1/FAK signaling to suppress migration and invasion by glioblastoma cells.\",\"authors\":\"Zhaoying Zhu, Yanjia Hu, Feng Ye, Haibo Teng, Guoliang You, Yunhui Zeng, Meng Tian, Jianguo Xu, Jin Li, Zhiyong Liu, Hao Liu, Niandong Zheng\",\"doi\":\"10.32604/or.2024.042456\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusions: </strong>IKIP inhibits THBS1/FAK signaling to suppress migration and invasion of GBM cells.</p>\",\"PeriodicalId\":19537,\"journal\":{\"name\":\"Oncology Research\",\"volume\":\"32 7\",\"pages\":\"1173-1184\"},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2024-06-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11211642/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Oncology Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.32604/or.2024.042456\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oncology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.32604/or.2024.042456","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
IKIP downregulates THBS1/FAK signaling to suppress migration and invasion by glioblastoma cells.
Background: 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.
Methods: 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.
Results: 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.
Conclusions: IKIP inhibits THBS1/FAK signaling to suppress migration and invasion of GBM cells.
期刊介绍：
Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.
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