不同EMT程序驱动的肿瘤异质性
肿瘤异质性相关研究揭示了不同EMT（上皮-间质转化）程序的关键作用。研究发现，PRRX1突变能影响肿瘤中EMT-T1和EMT-T2标记物的表达，同时伴随促炎性巨噬细胞的浸润，这显示了EMT-T1和EMT-T2在分别调控肿瘤细胞侵袭和炎症过程中的独特作用。进一步的分析通过多个模型数据，阐述了两种类似发育性或成人损伤相关的EMT程序，它们以不同方式激活炎症或侵袭性，协同推动肿瘤的发生和发展。这些重要发现为深入理解肿瘤异质性及探索新型靶向疗法提供了宝贵视角。
T细胞耗竭与“表观遗传疤痕”
患者对免疫检查点抑制剂等治疗方案的无应答状态中，实体肿瘤内部CD8 T细胞耗竭现象尤为突出，成为亟待解决的关键障碍。耗竭T细胞展现出一种特殊的表观遗传特征——表观遗传疤痕（epigenetic scarring），该特征即便在去除长期抗原刺激后依旧持续存在。理解不同染色质修饰因子之间的协同调控机制，确定它们所调控的关键基因如何介导效应T细胞的功能，将成为研究的重中之重。
甲硫氨酸循环与肿瘤进程
甲硫氨酸作为一种含硫的必需氨基酸，在人体内众多生化反应中发挥着重要作用。早期研究认为，甲硫氨酸仅是蛋白质合成的起始氨基酸；然而，随着研究的深入，人们逐渐发现它还广泛参与多种生物功能及相互关联的生化途径。本文旨在聚焦甲硫氨酸代谢在肿瘤发生与发展领域的最新研究成果。将深入探讨新近发现的依赖甲硫氨酸的生化通路及其驱动肿瘤生长的机制，并着重阐述利用甲硫氨酸循环作为创新疗法来治疗肿瘤的广阔前景。
网盘提示“本地路径无效，请检查本地下载路径”的另一种解决方法
前一天使用网盘能正常下载数据，第二天再用的时候提示“本地路径无效，请检查本地下载路径”。网上搜到的“文件夹名称过长，换个路径”“单个右击下载，不要批量”方案一一试过之后，全都无效。最后发现是程序自动升级后的版本有bug，可能与电脑系统出现了不兼容。卸载后重装旧版本，并阻止自动升级，就一切正常了。
点击化学与抗肿瘤药物设计
先驱转录因子PU.1在急性髓系白血病（AML）关键增强子的形成中起早期核心作用，与SWI/SNF协同推动MYC等关键致癌基因的表达。通过抑制SWI/SNF或干扰PU.1与DNA的结合，可有效破坏AML中的增强子结构，导致肿瘤细胞分化与增殖抑制。靶向PU.1-SWI/SNF调控轴为肿瘤精准治疗提供了新的方向。结合CUT&Tag与点击化学（Click Chemistry）开发的“CLICK-on-CUT&Tag”技术为精准识别PU.1功能靶点并诱导转录因子重新分布提供了有力工具。
Genetic Compensation Response in CRISPR-Based Gene Function Studies
Why does the same gene cause a phenotypic change when knocked down but not when knocked out? The disconnection between genotype and expected phenotype in such cases may be attributed to the activation of the Genetic Compensation Response (GCR). When a gene is mutated or knocked out, GCR is triggered, compensating for the lost function by upregulating homologous or functionally similar genes. This response is particularly pronounced when the mRNA contains a premature termination codon (PTC). GCR is not only a protective mechanism ensuring genetic robustness, but it may also play a significant role in influencing cancer progression. Understanding the mechanisms behind GCR is crucial for advancing our knowledge of tumor progression and for identifying new therapeutic targets.
Principles, Evolution, and Applications of Proximity Labeling
Proximity Labeling (PL) technology utilizes specific enzymes to covalently link labels (such as biotin) to proteins near the target protein, enabling the labeling and subsequent analysis of adjacent proteins. This labeling can be detected by mass spectrometry, revealing interactions between proteins. The advent of this technique has not only provided new tools and perspectives for studying protein-protein interactions but has also greatly advanced our understanding of critical biological processes such as cellular signaling and metabolic regulation.
Differences Between U6, EF1α, and Ubc Promoters
The U6 promoter originates from the RNA polymerase III (Pol III) system and is used to drive the expression of non-coding RNAs. Its most common applications include driving the expression of small RNA molecules such as short hairpin RNA (shRNA) and small guide RNA (sgRNA). If you need to express short RNA molecules like shRNA or sgRNA for RNA interference (RNAi) or CRISPR gene editing, the U6 promoter is the best choice. For efficiently and stably expressing exogenous proteins in a variety of cell lines, the EF1α promoter is a powerful and durable option, especially suited for long-term expression in lentiviral vector systems. The Ubc promoter is ideal for applications requiring stable gene expression with moderate strength, particularly in experiments where immunogenicity is a concern, such as with stem cells or primary cells.