相关实验视频

Updated: Jun 15, 2025

Correlating Gene-specific DNA Methylation Changes with Expression and Transcriptional Activity of Astrocytic KCNJ10 Kir4.1

Correlating Gene-specific DNA Methylation Changes with Expression and Transcriptional Activity of Astrocytic KCNJ10 Kir4.1

Published on: September 26, 2015

复发性结质母细胞瘤中的DNA甲基化:增加TEM8表达激活Src/PI3K/AKT/GSK-3β/B-Catenin通路

Paramita Kundu^1,2, Ruchi Jain^1,3, Nandaki Nag Kanuri⁴

¹Department of Molecular Reproduction, Development and Genetics, Indian Institute of Science, Bangalore, India.

Cancer genomics & proteomics

|August 27, 2024

概括

复发性质母细胞瘤显示全基因组DNA甲基化变化,包括改变TEM8的表达,这推动了瘤的进展和治疗耐药性. 这些表观遗传变化是理解质母细胞瘤复发的关键.

科学领域:

神经瘤学神经瘤学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
癌症生物学癌症生物学

背景情况:

质母细胞瘤 (GBM) 是一种具有攻击性的脑瘤,在治疗后经常复发.
在GBM中观察到治疗诱导的细胞可塑性和DNA损伤反应.
瘤异质性有助于治疗耐药性和疾病复发.

研究的目的:

与原发性瘤相比,研究复发性质母细胞瘤中的全基因组DNA甲基化变化.
为了确定与治疗暴露,耐药性和GBM复发相关的表观遗传变化.

主要方法:

用全基因组DNA甲基化阵列来比较11个初级GBM和13个复发的GBM.
差异甲基化分析确定了在复发瘤中受到影响的特定基因类别.
在关键的鉴定基因上进行了功能性研究 (过度表达,淘汰).

主要成果:

在反复发生的GBM中,确定了1,224个高甲基化和526个低甲基化探针.
在溶解物载体,离子通道,互白素受体/连接体,瘤抑制剂和转移相关基因中观察到差异甲基化.
在复发性GBM中,TEM8 (ANTXR1) 基因被低甲基化和上调,通过β-catenin通路激活促进了扩散,入侵,迁移和化学辐射抵抗.

结论:

在复发的GBM中,全基因组DNA甲基化变化是明显的.
在GBM的复发和进展中,TEM8基因起着重要作用.
TEM8通过调节β-catenin通路来影响GBM的攻击性.

关键词:

通过DNA甲基化.质母细胞瘤 (glioblastoma) 是一种复发性复发性复发性电阻的阻力可以瘤内皮标记物 8 瘤内皮标记物 8 这是一种β-catenin.

更多相关视频

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures

Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures

Published on: January 9, 2019

相关概念视频

mTOR Signaling and Cancer Progression

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

Epigenetic Regulation

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...