Genes & Diseases最新文献

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Intratumoral microenvironment remodeling by lncRNA ROLLCSC enhances lung adenocarcinoma progression lncRNA ROLLCSC对瘤内微环境的重塑促进肺腺癌的进展

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-08-05 DOI: 10.1016/j.gendis.2025.101788

Yu-Han Zhang , Jia-Cheng Xie , Ting Ye , Shi-Meng Guo , Xue Han , Si Yang , Lei Shi , Yi-Shi Li , H. Rosie Xing , Jing-Yu Li , Jian-Yu Wang

Metabolic reprogramming is one of the eight hallmarks of cancer, and in lung cancer, it is notably linked to ferroptosis-related lipid metabolism. Cancer stem cells, regarded as the initiating cells of cancer, can extensively influence the tumor microenvironment (TME). Nevertheless, their role in metabolic reprogramming within lung adenocarcinoma (LUAD) remains incompletely explored. In this study, through molecular biology experiments including RNA-seq, proteomics, RNA pulldown, and PCR, we discovered a novel and intricate mechanism by which the lncRNA ROLLCSC, derived from extracellular vesicles (EVs) of LUAD stem cells, regulates the tumor TME. Mechanistically, lncRNA ROLLCSC can interact with CDC42, a GTPase protein, mediating a positive feedback loop that promotes the entry of more EVs into recipient lung cancer cells (LLC). FTO-mediated m6A demethylation enhances the stability of ROLLCSC, which is recognized by the reader protein IGF2BP2 in recipient LLC cells. Most importantly, lncRNA ROLLCSC can reshape the lipid metabolism of LLC cells by targeting ACSL4 and Slc25a11, thereby enhancing their resistance to ferroptosis. Clinically, ROLLCSC and its targets are associated with distinct tumor expression patterns and have prognostic significance. Overall, our study elucidates how the lncRNA ROLLCSC derived from cancer stem cell (CSC)-derived EVs is efficiently transported to LUAD cells, subsequently reshaping the lipid metabolism of recipient cells and enhancing their resistance to ferroptosis.

代谢重编程是癌症的八大特征之一，在肺癌中，它与铁中毒相关的脂质代谢密切相关。肿瘤干细胞作为肿瘤的起始细胞，可以广泛影响肿瘤微环境（tumor microenvironment， TME）。然而，它们在肺腺癌（LUAD）代谢重编程中的作用仍未完全探索。本研究通过RNA-seq、蛋白质组学、RNA pulldown、PCR等分子生物学实验，发现了LUAD干细胞细胞外囊泡（EVs）衍生的lncRNA ROLLCSC调控肿瘤TME的一种新颖而复杂的机制。在机制上，lncRNA ROLLCSC可以与CDC42（一种GTPase蛋白）相互作用，介导一个正反馈循环，促进更多ev进入受体肺癌细胞（LLC）。fto介导的m6A去甲基化增强了ROLLCSC的稳定性，这在受体LLC细胞中被读取器蛋白IGF2BP2识别。最重要的是，lncRNA ROLLCSC可以通过靶向ACSL4和Slc25a11重塑LLC细胞的脂质代谢，从而增强LLC细胞对铁下垂的抵抗力。在临床上，ROLLCSC及其靶点与不同的肿瘤表达模式相关，具有预后意义。总的来说，我们的研究阐明了来自癌症干细胞（CSC）来源的ev的lncRNA ROLLCSC如何有效地转运到LUAD细胞，随后重塑受体细胞的脂质代谢并增强其对铁凋亡的抵抗力。

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引用次数: 0

Genetic characteristics and prognosis of m6A RNA methylation regulator in acute myeloid leukemia 急性髓性白血病中m6A RNA甲基化调控因子的遗传特征及预后

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-08-05 DOI: 10.1016/j.gendis.2025.101789

Kaili Liao , Daixin Guo , Yujie Hu , Jiarong Wen , Yuhan Xu , Xinyi Bai , Jinting Cheng , Beining Zhang , Xiaozhong Wang

引用次数: 0

cGAS knockout inhibited endotoxin-induced uveitis in mice cGAS敲除抑制内毒素诱导的小鼠葡萄膜炎

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-29 DOI: 10.1016/j.gendis.2025.101786

Yue Guo , Ruiping Gu , Jiaojiao Wei , Chunhui Jiang

Our research focused on the impact of the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)–stimulator of interferon genes (STING) pathway on retinal inflammation and employed an endotoxin-induced uveitis (EIU) model. EIU was provoked in mice through the intravitreal administration of lipopolysaccharide. Transcriptome analysis was performed via bulk RNA sequencing. Cytosolic mitochondrial DNA levels in the retina were quantified via PCR. Western blotting was used to assess the activation of cGAS‒STING signaling at specified times after intravitreal lipopolysaccharide injection. To understand the influence of the cGAS‒STING pathway on inflammatory retinal disorders, Cgas knockout mice were developed. Fundus imaging and fluorescein angiography were conducted to observe vitreous inflammation. Microstructural analysis of the eyes was performed, and histopathological scoring was performed. Retinal leukocytosis assays were used to evaluate retinal inflammation. Analysis of these differentially expressed mRNAs revealed activation of the cGAS‒STING signaling pathway, which was confirmed by western blotting analysis of these proteins. Using Cgas knockout mice, we observed significant inhibition of endotoxin-induced intraocular inflammation, including reduced vitreous inflammation, reduced retinal vascular leakage, decreased leukocyte adhesion, inhibited infiltration and activation of macrophages in the retina, and inhibited microglial activation. These findings suggest that cGAS might be a potential novel therapeutic target for uveitis.

我们的研究重点是环鸟苷-单磷酸腺苷合成酶(cGAS) -干扰素基因刺激因子（STING）通路对视网膜炎症的影响，并采用内毒素诱导的葡萄膜炎（EIU）模型。通过玻璃体内给药脂多糖引起小鼠EIU。转录组分析通过大量RNA测序进行。通过PCR定量测定视网膜胞质线粒体DNA水平。采用Western blotting检测玻璃体内注射脂多糖后特定时间cGAS-STING信号的激活情况。为了了解Cgas - sting通路对炎症性视网膜疾病的影响，我们培育了Cgas敲除小鼠。眼底造影及荧光素血管造影观察玻璃体炎症。进行眼部显微结构分析，并进行组织病理学评分。视网膜白细胞计数法评估视网膜炎症。对这些差异表达mrna的分析显示，cGAS-STING信号通路被激活，这一点通过对这些蛋白的western blotting分析得到了证实。通过Cgas敲除小鼠，我们观察到内毒素诱导的眼内炎症有明显的抑制作用，包括减少玻璃体炎症，减少视网膜血管渗漏，减少白细胞粘附，抑制视网膜巨噬细胞的浸润和活化，抑制小胶质细胞的活化。这些发现表明，cGAS可能是葡萄膜炎的一个潜在的新治疗靶点。

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引用次数: 0

Lactylation-driven METTL3 regulates wound healing by enhancing m6A/HNRNPA2B1/DNMT1 signaling in keratinocytes 乳酸化驱动的METTL3通过增强角质形成细胞中的m6A/HNRNPA2B1/DNMT1信号来调节伤口愈合

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-28 DOI: 10.1016/j.gendis.2025.101787

Xue-ting Hu , Lu-min Sui , Cheng-xiu Pu , Luo-quan Ao , Mu Yuan , Li Deng , Qing Zhao , Xiao-feng Wu , Xiang Xu

引用次数: 0

Non-clinical safety considerations on genome editing using the CRISPR/Cas system 使用CRISPR/Cas系统进行基因组编辑的非临床安全性考虑

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-28 DOI: 10.1016/j.gendis.2025.101785

Parto Toofan, Mark Singh, Andrew Brooks, Keith McLuckie

Recent advances in gene editing using the CRISPR/Cas system have revolutionized genome editing, opening new horizons for human cellular and gene therapy products. Genome editing technologies are rapidly being adopted in clinical trials. However, critical non-clinical safety considerations are required to address challenges in translating research to the clinic. Here, we review current ex vivo and in vivo genome editing approaches using the CRISPR/Cas system and discuss the practical use of these methods in pre-clinical studies and in the clinic. We also discuss known limitations of genome editing in humans and the mitigation of risk factors associated with it from a non-clinical safety perspective. This review aims to aid researchers in acquiring a perspective that is essential for the safe translation of genome editing to the clinic.

利用CRISPR/Cas系统进行基因编辑的最新进展使基因组编辑发生了革命性的变化，为人类细胞和基因治疗产品开辟了新的视野。基因组编辑技术正在迅速应用于临床试验。然而，在将研究转化为临床时，需要考虑关键的非临床安全性问题。在这里，我们回顾了目前使用CRISPR/Cas系统的离体和体内基因组编辑方法，并讨论了这些方法在临床前研究和临床中的实际应用。我们还从非临床安全的角度讨论了人类基因组编辑的已知局限性以及与之相关的风险因素的缓解。这篇综述旨在帮助研究人员获得对基因组编辑安全转化为临床至关重要的观点。

引用次数: 0

Identification and functional characterization of a novel nonsense mutation of CASR gene in a familial hypocalciuric hypercalcemia pedigree 家族性低钙高钙血症家系中CASR基因新无义突变的鉴定和功能表征

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-25 DOI: 10.1016/j.gendis.2025.101781

Yang Tian , Bingyang Liu , Yang Xudan , Ruojun Qiu , Zhang Shaojun , Huang Haoshu , Wu Fang , Fenping Zheng

引用次数: 0

CBS promotes tumor immune evasion by reducing MHC-I stability CBS通过降低MHC-I的稳定性促进肿瘤免疫逃避

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-25 DOI: 10.1016/j.gendis.2025.101782

Yanrong Yang , Yadong Guo , Shiyu Mao , Chengyuan Dong , Zhu Yu , Xudong Yao , Bing Shen

引用次数: 0

NAD+ supplementation augments the efficacy of the PARP1 inhibitor PJ34 in a 6-OHDA-induced model of Parkinson’s disease 在6-羟多巴胺诱导的帕金森病模型中，补充NAD+可增强PARP1抑制剂PJ34的疗效

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-25 DOI: 10.1016/j.gendis.2025.101783

Mengling Hu , Xiaoqian Li , Dongsheng Fan , Lu Yu , Fan Ren , Jianming Wu , Jianing Mi , Yang Zheng , Xiaogang Zhou , Dalian Qin , Anguo Wu

引用次数: 0

cTnIR193H restrictive cardiomyopathy mice satisfy high-energy metabolic demands through regulating glucose metabolism cTnIR193H限制性心肌病小鼠通过调节葡萄糖代谢来满足高能代谢需求

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-25 DOI: 10.1016/j.gendis.2025.101784

Min Luo , Lingjuan Liu , Wenjing Yuan , Junjun Quan , Mi Li , Jie Tian

This work aims to investigate the energy metabolism in mice with restrictive cardiomyopathy induced by cardiac troponin I (cTnI) R193H mutation. Echocardiography was used to monitor cardiac function. ATP content and ATPase activity were detected with relevant kits. The expression levels of GLUT4, FAT/CD36, and PI3K/AKT pathway proteins were detected. Proteomics and phosphorylation omics were used to analyze the differential expression and modification of cardiac proteins and related pathways, respectively. The utilization of cardiac energy substrates was investigated using relevant kits. The isovolumic relaxation time of 4-month-old cTnI193His-M mice was significantly prolonged (P < 0.01); Cardiac ATP content, ATPase activity, and mitochondrial number were significantly increased (P < 0.05, P < 0.01, and P < 0.01, respectively); GLUT4 expression level increased (P < 0.01); the expression level of CD36 decreased (P < 0.01). Proteomic results showed that the glycolytic/gluconeogenic pathway was up-regulated. Phosphorylation omics was enriched in the inositol phosphate metabolism pathway and PI3K/AKT pathway. In conclusion, at the early stage of diastolic dysfunction, cTnI193His-M mice may increase glucose uptake and metabolism through the PI3K/AKT pathway to satisfy the high energy demand, which may contribute to the development of myocardial fibrosis and heart failure.

本研究旨在探讨心肌肌钙蛋白I (cTnI) R193H突变致限制性心肌病小鼠的能量代谢。超声心动图监测心功能。用相关试剂盒检测ATP含量和ATP酶活性。检测GLUT4、FAT/CD36、PI3K/AKT通路蛋白的表达水平。蛋白质组学和磷酸化组学分别分析了心脏蛋白和相关途径的差异表达和修饰。采用相关试剂盒对心能底物的利用情况进行了研究。4月龄cTnI193His-M小鼠等容松弛时间明显延长（P < 0.01）；心肌ATP含量、ATP酶活性和线粒体数量显著升高（P < 0.05、P <； 0.01和P <； 0.01）；GLUT4表达水平升高（P < 0.01）；CD36表达水平降低（P < 0.01）。蛋白质组学结果显示糖酵解/糖异生通路上调。磷酸化组学富集于肌醇磷酸代谢途径和PI3K/AKT途径。综上所述，在舒张功能障碍早期，cTnI193His-M小鼠可能通过PI3K/AKT通路增加葡萄糖摄取和代谢，以满足高能量需求，这可能有助于心肌纤维化和心力衰竭的发展。

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引用次数: 0

Unveiling the roles of SPP1+ macrophage and IGFBP2+ fibroblast in lung adenosquamous carcinoma through single-cell analysis 通过单细胞分析揭示SPP1+巨噬细胞和IGFBP2+成纤维细胞在肺腺鳞癌中的作用

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-24 DOI: 10.1016/j.gendis.2025.101779

Yao Lin , Yaxin Chen , Dandan Xiong , Jing Huang , Hongmo Liu , Yawen Qi , Jinfeng Chen , Jun Meng , Yueqi Li , Jingyuan Yang , Yi Bao , Wenxing Li , Li Yang , Sanqi An

引用次数: 0

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