NUCLEAR FACTOR-KAPPAB IN CANCER DEVELOPMENT AND PROGRESSION

核因子-KAPPAB 在癌症发生和进展中的作用

• 批准号: 7722467
• 负责人: Michael Karin
• 金额: $ 0.1万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-05-01 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7722467
• 关键词: Apoptosis; Autophagocytosis; Cell Death; Cells; Chemopreventive Agent; Complex; Computer Retrieval of Information on Scientific Projects Database; Condition; Development; Eating; Electron Microscopy; Funding; Grant; Immune response; Inflammation; Institution; Link; Malignant Neoplasms; Mediating; Medical Surveillance; Mitochondria; Nuclear; Pathway interactions; Research; Research Personnel; Resources; Role; Signal Pathway; Signal Transduction; Source; Tumor Angiogenesis; United States National Institutes of Health; base; biological adaptation to stress; cancer cell; killings; neoplastic; transcription factor; tumor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Nuclear factor-kappaB (NF-kappaB) transcription factors and the signaling pathways that activate them are central coordinators of innate and adaptive immune responses. It has become clear that NF-kappaB signaling also has a critical role in cancer development and progression. NF-kappaB provides a mechanistic link between inflammation and cancer, and is a major factor controlling the ability of both pre-neoplastic and malignant cells to resist apoptosis-based tumor-surveillance mechanisms. NF-kappaB might also regulate tumor angiogenesis and invasiveness, and the signaling pathways that mediate its activation provide attractive targets for new chemopreventive and chemotherapeutic approaches. With inflammation-linked cancers, the functional relationship between apoptosis ('self-killing') and autophagy ('self-eating') is complex because under certain circumstances, autophagy is a stress response that avoids cell death and suppresses apoptosis, whereas under other conditions, it constitutes an alternative cell-death pathway. Because mitochondria are key players in apoptosis, we are using the electron microscopy resources of NCMIR to investigate potential structural changes to mitochondria indicative of signaling pathways related to a cell's apoptosis-based tumor-surveillance mechanisms.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 核因子-κ B（NF-kappaB）转录因子和激活它们的信号通路是先天性和适应性免疫应答的中心协调者。已经清楚的是，NF-κ B信号传导在癌症的发展和进展中也起着关键作用。NF-kappaB提供了炎症和癌症之间的机制联系，并且是控制癌前细胞和恶性细胞抵抗基于细胞凋亡的肿瘤监视机制的能力的主要因素。NF-kappaB还可能调节肿瘤血管生成和侵袭性，并且介导其活化的信号通路为新的化学预防和化学治疗方法提供了有吸引力的靶点。对于与炎症相关的癌症，细胞凋亡（“自我杀死”）和自噬（“自我吞噬”）之间的功能关系很复杂，因为在某些情况下，自噬是一种避免细胞死亡并抑制细胞凋亡的应激反应，而在其他情况下，它构成了另一种细胞死亡途径。由于线粒体是细胞凋亡中的关键参与者，我们正在使用NCMIR的电子显微镜资源来研究线粒体的潜在结构变化，这些结构变化指示与细胞凋亡相关的肿瘤监视机制的信号通路。