相关实验视频

Updated: Jul 13, 2025

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

干扰TM4SF3与AR或AR-V7相互作用的类蛋白阻断前列腺癌细胞增殖

Prabesh Khatiwada^1,2, Ujjwal Rimal¹, Mamata Malla¹

¹Department of Biological Sciences, University of Toledo, Toledo, Ohio, USA.

Endocrine oncology (Bristol, England)

|October 12, 2023

概括

针对雄激素受体 (AR) 和超膜4超家族3 (TM4SF3) 相互作用的新型可以杀死前列腺癌细胞,包括对恩扎胺抗性割抗性前列腺癌 (CRPC).

科学领域:

在瘤学瘤学.
分子生物学分子生物学
药物发现药物发现药物发现

背景情况:

雄激素受体 (AR) 信号驱动前列腺癌进展到割抵抗性前列腺癌 (CRPC).
AR拼接变体 (AR-Vs) 导致CRPC中异常的AR激活和耐药性.
准蛋白质与蛋白质相互作用是一个有前途的治疗策略.

研究的目的:

通过使用设计来研究破坏AR/TM4SF3相互作用的潜力.
评估这些在杀死前列腺癌细胞,包括耐药形式的有效性.

主要方法:

确定AR和AR-V7与TM4SF3的相互作用,并绘制最小相互作用区域的地图.
针对这些相互作用域的 (TA1,AT1) 的设计和合成.
对AR/TM4SF3相互作用,基因调节,细胞活力,细胞亡,迁移和转变的效应的评估.

主要成果:

酸TA1和AT1降低了AR/TM4SF3蛋白的相互作用和稳定性.
TA1抑制了AR/TM4SF3对基因促进物和下调的AR基因的招募.
这两种都对表达AR和AR-V7的前列腺癌细胞表现出细胞毒性,TA1在耐恩扎胺模型中显示出有效性.
TA1还抑制了细胞迁移和恶性转变.

结论:

针对AR/TM4SF3与的相互作用,为前列腺癌提供了一种新的治疗方法.
TA1显示出治疗酶胺耐药CRPC的显著潜力,这表明了新的治疗途径.

关键词:

这就是为什么AR AR AR AR.在AR-V7中使用AR-V7.在TM4SF3中,我们可以使用TM4SF3.酸是一种酸.前列腺癌是前列腺癌.

更多相关视频

MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent

MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent

Published on: September 3, 2013

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

Mitogens and the Cell Cycle

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

Targeted Cancer Therapies

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...