相关实验视频

Updated: Jun 17, 2025

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark

Published on: January 26, 2018

H3K18 乳化增强了非小细胞肺癌的免疫逃生

Cai Zhang^1,2, Lijie Zhou³, Mingyuan Zhang⁴

¹Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Cancer research

|August 13, 2024

概括

基斯乳化驱动非小细胞肺癌通过增强PD-L1表达来驱动免疫逃避. 用代谢抑制剂和免疫疗法向这种表观遗传修饰显示出癌症治疗的希望.

科学领域:

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
免疫学免疫学免疫学

背景情况:

氨酸乳化是一种涉及癌症发展的表观遗传修饰.
基斯乳化可能会影响瘤的微环境和免疫规避.
非小细胞肺癌 (NSCLC) 呈现高乳化.

研究的目的:

调查素H3素18乳化 (H3K18la) 在NSCLC进展和免疫逃避中的作用.
阐明H3K18la促进免疫逃生的分子机制.
评估针对NSCLC中的H3K18la的治疗策略.

主要方法:

在NSCLC组织中分析H3K18la水平和与预后的相关性.
抑制糖解和乳酸脱酶 (LDH) A/B,以评估对H3K18la和T细胞细胞毒性的影响.
通过H3K18la.la.对POM121/MYC/PD-L1通路激活的研究.
在小鼠NSCLC异种移植模型中对组合疗法 (糖解抑制剂和抗PD-1抗体) 的评估.

主要成果:

在NSCLC中H3K18la水平升高与预后不佳相关.
糖解抑制和LDH沉默降低了H3K18la,并增强了CD8+T细胞细胞毒性.
发现H3K18la激活了POM121转录,增强了MYC介导的PD-L1表达.
组合疗法通过促进内CD8+T细胞功能,显示出显著的抗瘤疗效.

结论:

H3K18la通过POM121/MYC/PD-L1途径促进NSCLC的免疫逃生.
代谢重编程和免疫疗法可以逆转H3K18la诱导的免疫抑制.
向H3K18la代表了NSCLC治疗的潜在表观遗传策略.

更多相关视频

Patient-Derived Tumor Explants As a "Live" Preclinical Platform for Predicting Drug Resistance in Patients

Patient-Derived Tumor Explants As a "Live" Preclinical Platform for Predicting Drug Resistance in Patients

Published on: February 7, 2021

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

相关概念视频

lncRNA - Long Non-coding RNAs

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...

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...

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...

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...