NEW METASTASIS SUPPRESSOR GENE

新的转移抑制基因

• 批准号: 2700684
• 负责人: Emma Shtivelman
• 金额: $ 24.28万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-05-01 至 2000-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2700684
• 关键词: SCID mouse; angiogenesis; cell adhesion; disease /disorder model; gene expression; human fetus tissue; immunofluorescence technique; immunoprecipitation; metastasis; model design /development; neoplasm /cancer classification /staging; neoplasm /cancer genetics; neoplastic process; oncoproteins; posttranslational modifications; prognosis; protein structure function; small cell lung cancer; tumor suppressor genes

DESCRIPTION: (adapted from the investigator's abstract) Mechanisms of metastatic spread of high aggressive tumors such as small cell lung cancer (SCLC) are poorly understood. A unique SCID-hu metastasis model was developed that for the first time allows metastasis of SCLC to be studied in the experimental in vivo setting. Molecular analysis of SCLC cell lines with different metastatic potentials have led to the identification of a novel human gene designated CC3 whose expression is lacking in metastatic cells. Introduction of CC3 into SCLC cells suppresses their ability to form metastatic tumors in the SCID-hu mice. The goal of this project then is to prove that CC3 is a metastasis suppressor gene in small cell lung cancer and to analyze the mechanisms of metastasis suppression by CC3. The functional relevance of the lack of expression of CC3 to the metastatic phenotype of SCLC will be further confirmed in the in vivo metastasis assays. The clinical relevance and potential prognostic significance of CC3 expression will be evaluated through analysis of its expression in clinical tumor specimens. The mechanism of metastasis-suppression by CC3 will be addressed in experiments designed to define the effects of CC3 expression on the phenotype of metastatic cells. These investigators anticipate that the results of these studies will advance the understanding of the mechanisms of metastasis of SCLC. Lack of CC3 protein could have prognostic significance in patients diagnosed with SCLC and potentially other tumors. A thorough understanding of CC3 function might eventually lead to the development of new anti-metastatic therapies.

描述：（改编自研究者摘要） 高侵袭性肿瘤如小细胞肺癌的转移扩散 （SCLC）知之甚少。 一种独特的SCID-hu转移模型， 首次允许研究SCLC的转移， 体内实验环境。 SCLC细胞系的分子分析 不同的转移潜能导致了一种 命名为CC 3的新的人类基因，其表达在转移性肿瘤中缺乏。 细胞 将CC 3引入SCLC细胞抑制其形成 SCID-hu小鼠中的转移性肿瘤。 这个项目的目标是 证明CC 3是小细胞肺癌转移抑制基因， 分析CC 3抑制肿瘤转移的机制。 功能 CC 3表达缺失与肺癌转移表型的相关性 SCLC将在体内转移测定中进一步证实。 的 CC 3表达的临床相关性和潜在预后意义 将通过分析其在临床肿瘤中的表达来评估 标本 CC 3抑制肿瘤转移的机制将被阐明 在设计用于确定CC 3表达对细胞凋亡的影响的实验中， 转移细胞的表型。 这些研究人员预计， 这些研究的结果将促进对 小细胞肺癌的转移。 CC 3蛋白缺失可能具有预后意义 诊断为SCLC和其他潜在肿瘤的患者。 的透彻 对CC 3功能的理解可能最终导致 新的抗转移疗法