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Chemotactic Formylpeptide Receptor DevelopmentProgression Malignant Human Gliom

Chemotactic Formylpeptide Receptor DevelopmentProgression Malignant Human Gliom
趋化甲酰肽受体的发育进展人类恶性胶质瘤
批准号：
7592882
负责人：
JI MING WANG
金额：
$27.05万
依托单位：
DIVISION OF BASIC SCIENCES - NCI
依托单位国家：
美国
项目类别：
财政年份：
--
资助国家：
美国
项目状态：
未结题
起止时间：
至
来源：
https://reporter.nih.gov/project-details/7592882
关键词：
AgonistCell CommunicationCell Differentiation processCellsChemotaxisCoupledEnvironmentG-Protein-Coupled ReceptorsGlioblastomaGliomaHumanMalignant - descriptorMolecularNecrosisNude MiceProductionRNA InterferenceRegulationRoleSignal TransductionSignal Transduction PathwaySmall Interfering RNASpecimenTumorigenicityVascular Endothelial Growth FactorsXenograft Modelknock-downmalignant phenotypeneoplastic cellreceptorselective expressionsensortumortumor progressiontumorigenesis

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中文摘要
翻译
我们发现一种g蛋白偶联受体FPR在高度恶性的人胶质母细胞瘤细胞中选择性表达。FPR的激活促进肿瘤细胞趋化、存活和血管生成因子VEGF的产生。通过小干扰RNA敲除FPR可显著降低裸鼠胶质母细胞瘤细胞形成肿瘤的能力。此外，FPR被坏死肿瘤细胞上清中含有的激动剂活性激活。因此，FPR作为胶质母细胞瘤细胞的传感器，在肿瘤环境中产生激动剂，从而加剧肿瘤的进展。
英文摘要
We have found that a G-protein coupled receptor FPR is selectively expressed by highly malignant human glioblastoma cells. Activation of FPR promotes tumor cell chemotaxis, survival and production of angiogenic facotr VEGF. Knocking down FPR by small interfering RNA markedly reduces the capacity of glioblastoma cells to form tumors in nude mice. In addition, FPR is activated by agonist activity contained in the supernatants of necrotic tumor cells. Thus, FPR acts as a sensor on glioblastoma cells for agonists produced in the tumor environment to exacerbate the progression of the tumor.
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