相关实验视频

Updated: Jul 17, 2025

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

抗氧化剂刺激了依赖BACH1的瘤血管生成

Ting Wang¹, Yongqiang Dong², Zhiqiang Huang¹

¹Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.

The Journal of clinical investigation

|August 31, 2023

概括

转录因子BACH1通过控制关键基因促进肺癌血管生成. 抗氧化剂促进了这一过程,突出了BACH1作为肺癌潜在的治疗点.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

肺癌的进展与血管生成有关,即新血管的形成.
缺氧诱导因素 (HIFs) 通常调节血管生成,但其他因素也参与其中.
红氧敏感转录因子在瘤血管生成中的作用越来越被认可.

研究的目的:

调查BTB和CNC同质性1 (BACH1) 在控制肺癌中的血管生成基因转录中的作用.
为了确定BACH1是否在调节血管生成时独立于HIFs起作用.
探索针对BACH1及其相关途径的治疗潜力.

主要方法:

评估了BACH1对肺癌细胞,有机体和异种移植中的血管生成基因的控制.
在正常和缺氧状态下服用抗氧化剂 (维生素C和E,N-乙半氨酸).
使用了BACH1-过度表达和淘汰细胞模型.
研究了BACH1作为HIF1α的转录标.
在患者瘤样本中分析了BACH1表达.

主要成果:

BACH1调节了一系列血管生成基因.
在normoxia下,抗氧化剂以BACH1依赖的方式增加了血管生成基因表达.
BACH1水平是由低氧和酸酶抑制剂调节的.
BACH1是HIF1α的标,但其益血管性活性是独立于HIF1α的.
增加的BACH1表达与患者瘤中的血管新生标志物相关,以及对抗血管新生疗法敏感的瘤.

结论:

BTB和CNC同质性1 (BACH1) 是肺癌血管生成的关键氧和氧化复原敏感转录因子.
向BACH1或调节氧化还原平衡是肺癌抗血管生成疗法的有希望的策略.

关键词:

血管新生的产生.氧气过低是因为缺氧.肺癌是一种肺癌.

更多相关视频

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells

Monitoring Functionality and Morphology of Vasculature Recruited by Factors Secreted by Fast-growing Tumor-generating Cells

Published on: November 23, 2014

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

相关概念视频

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...

Mechanism of Angiogenesis

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...

Electron Transport Chain: Complex I and II

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

The Tumor Microenvironment

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...