Genes & Diseases最新文献

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MiR-378 mediates the ovariectomy induced bone loss via exaggerating osteoclastogenesis and transforming growth factor beta impaired osteogenesis MiR-378通过促进破骨细胞生成和转化生长因子β损伤成骨，介导卵巢切除术诱导的骨丢失

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-03 DOI: 10.1016/j.gendis.2025.101754

Lu Feng , Zhengmeng Yang , Nan Hou , Haixing Wang , Shanshan Bai , Xuan Lu , Yaofeng Wang , Sien Lin , Micky D. Tortorella , Gang Li

Osteoporosis (OP) is a disease characterized by decreased bone mass and damaged architectures. The promising treatment strategy for OP is to inhibit bone resorption while promoting bone formation. MicroRNAs (miRNAs) have been shown to be associated with osteoclastogenesis and osteogenesis processes in OP. In our previous study, we discovered that miR-378 inhibits bone marrow mesenchymal stem cell (BMSC) osteogenesis and bone formation during fracture healing. However, the role of miR-378 during OP progression is not validated. In this study, we found that miR-378 transgenic (Tg) mice exhibited excessive bone loss after ovariectomy (OVX) treatment. MiR-378 increased BMSC’s osteoclastogenesis by activating both canonical and non-canonical nuclear factor kappa-light-chain-enhancer of activated B (NFκB) signaling pathway. Tumor necrosis factor receptor-associated factor 3 (Traf3) was directly regulated by miR-378 during osteoclast differentiation. miR-378 also aggravated transforming growth factor beta (TGFβ) impaired osteogenesis upon OVX treatment. Traf3 was involved in this process as well. In in vivo study, the intravenous injection of anti-miR-378 lentivirus could significantly rescue OVX induced bone loss and bone microarchitecture impairment. This study uncovered the novel role of miR-378 in OVX induced osteoporosis. The potential of developing miRNA-378 inhibitors as novel diagnostics or blockers as therapeutics for osteoporosis is worth exploring.

骨质疏松症（OP）是一种以骨量减少和结构受损为特征的疾病。有希望的治疗策略是抑制骨吸收，同时促进骨形成。MicroRNAs （miRNAs）已被证明与op的破骨细胞发生和成骨过程相关。在我们之前的研究中，我们发现miR-378在骨折愈合过程中抑制骨髓间充质干细胞（BMSC）的成骨和骨形成。然而，miR-378在OP进展中的作用尚未得到证实。在这项研究中，我们发现miR-378转基因（Tg）小鼠在卵巢切除术（OVX）治疗后表现出过度的骨质流失。MiR-378通过激活活化B （NFκB）信号通路的典型和非典型核因子kappa-轻链增强子，增加BMSC的破骨细胞生成。肿瘤坏死因子受体相关因子3 （Tumor necrosis factor receptor-associated factor 3, Traf3）在破骨细胞分化过程中受到miR-378的直接调控。在OVX治疗后，miR-378也加重了转化生长因子β (TGFβ)的成骨功能受损。Traf3也参与了这个过程。在体内研究中，静脉注射anti-miR-378慢病毒可显著挽救OVX诱导的骨丢失和骨微结构损伤。这项研究揭示了miR-378在OVX诱导的骨质疏松症中的新作用。开发miRNA-378抑制剂作为骨质疏松症的新型诊断或阻滞剂的潜力值得探索。

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引用次数: 0

Single-cell molecular communications and transcriptional regulatory dynamics of T cell immunotherapy in bladder cancer 膀胱癌中T细胞免疫治疗的单细胞分子通讯和转录调控动力学

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-03 DOI: 10.1016/j.gendis.2025.101760

Limin Liu , Xuan Wan , Su Liu , Chenjie Yu , Hongman Xue , Jiayi Wang , Zhu Li , Kai Liu , Chun Chen , Jiajian Wang

引用次数: 0

EGFR A859S alteration may predict a better response to third-generation EGFR-TKI treatment in advanced NSCLC EGFR A859S改变可能预示着晚期NSCLC对第三代EGFR- tki治疗的更好反应

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-02 DOI: 10.1016/j.gendis.2025.101757

Weiping Hong, Wenfan Fu, Ya Ma, Chenxuan Wang, Yang Xu, Jiani Yin, Jiaohui Pang, Qiuxiang Ou, Hua Bao, Jincui Gu, Baoxiu Li

引用次数: 0

The role of m6A methylation in female reproductive physiology and pathology m6A甲基化在女性生殖生理和病理中的作用

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-07-01 DOI: 10.1016/j.gendis.2025.101755

Jie Ding , Yalun He , Yangshuo Li , Shuai Sun , Wen Cheng , Jiami Huang , Chaoqin Yu

N6-methyladenosine (m⁶A) is a critical regulator of female reproductive physiology, yet existing reviews have focused predominantly on oocytes. The objective of this review is to systematically evaluate the regulatory effects of m⁶A throughout the pregnancy process. This review covers aspects such as oocyte maturation, granulosa cell dynamics, endometrial receptivity, immune homeostasis, and systemic adaptations, aiming to demonstrate the comprehensive regulatory capacity of m⁶A in female reproduction. Dysregulated m⁶A modifications in infertility-associated pathologies, including endometriosis, polycystic ovary syndrome, and recurrent miscarriage, are analyzed to identify mechanistic links between an epitranscriptomic imbalance and reproductive dysfunction. The key findings indicate that m⁶A is involved in the entire reproductive process and precisely coordinates stage-specific molecular programs within it, whereas aberrant methylation patterns disrupt gene networks essential for fertility. Notably, m⁶A-modifying enzymes exhibit strong potential as diagnostic biomarkers for female reproductive disorders. The synthesis of the current evidence establishes m⁶A dysregulation as a convergent pathogenic mechanism in diverse infertility etiologies, suggesting that the therapeutic modulation of m⁶A pathways could address unmet clinical needs in reproductive medicine.

n6 -甲基腺苷（m6A）是女性生殖生理的重要调节因子，但现有的研究主要集中在卵母细胞上。本综述的目的是系统地评估m6A在整个妊娠过程中的调节作用。本文从卵母细胞成熟、颗粒细胞动力学、子宫内膜容受性、免疫稳态和系统适应等方面综述了m6A在女性生殖中的综合调控能力。研究人员分析了m6A在不孕相关疾病（包括子宫内膜异位症、多囊卵巢综合征和复发性流产）中的失调，以确定表转录组失衡和生殖功能障碍之间的机制联系。关键发现表明，m6A参与了整个生殖过程，并在其中精确地协调特定阶段的分子程序，而异常的甲基化模式破坏了生育所必需的基因网络。值得注意的是，m6a修饰酶作为女性生殖障碍的诊断生物标志物具有很强的潜力。综合目前的证据，确定m6A失调是多种不孕症病因的趋同致病机制，表明m6A通路的治疗性调节可以解决生殖医学未满足的临床需求。

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引用次数: 0

A systematic CRISPR screen reveals an NBL1-mediated Jak/Stat3 crosstalk to promote ovarian cancer metastasis 系统的CRISPR筛选揭示了nbl1介导的Jak/Stat3串扰促进卵巢癌转移

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-06-28 DOI: 10.1016/j.gendis.2025.101740

Yue Qi , Wenwen Zhang , Xinyu Li , Yi Shi , Pengpeng Qu

Patients with ovarian cancer (OC) are at high risk of developing transcoelomic metastasis in the early stages, which is strongly associated with increased mortality rates. However, the mechanism by which OC cells disseminate from the primary site and colonize distant sites remains unknown. Here, through an in vivo genome-wide CRISPR/Cas9 screen, we identified NBL1, which increased dramatically in OC patients during peritoneal metastasis, as a key factor promoting the transcoelomic metastasis of OC. Overexpression of NBL1 in OC cells greatly promotes the transcoelomic metastasis. When OC cells disseminate into the peritoneal cavity, they induce the transition of peritoneal epithelial cells to mesothelial cells, ultimately activating the Jak/Stat3 signaling pathway. Thus, we show a NBL1-mediated crosstalk between peritoneum epithelial cells and mesothelial cells that supports a metastasis-promoting process.

卵巢癌（OC）患者在早期阶段发生经结肠转移的风险很高，这与死亡率增加密切相关。然而，OC细胞从原发部位扩散并迁移到远处部位的机制尚不清楚。在这里，我们通过体内全基因组CRISPR/Cas9筛选，发现NBL1在OC患者腹膜转移过程中显著增加，是促进OC跨体腔转移的关键因素。NBL1在OC细胞中的过表达可显著促进肿瘤的跨体腔转移。当OC细胞扩散到腹膜腔时，诱导腹膜上皮细胞向间皮细胞转变，最终激活Jak/Stat3信号通路。因此，我们发现nbl1介导的腹膜上皮细胞和间皮细胞之间的串扰支持促进转移的过程。

引用次数: 0

Uncovering stromal cell fate genes and a novel risk stratification in UCEC by integrating single-cell RNA sequencing and multi-omics analysis 通过整合单细胞RNA测序和多组学分析，揭示间质细胞命运基因和UCEC的新风险分层

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-06-27 DOI: 10.1016/j.gendis.2025.101743

Rulin Zhang , Haonan Ma , Yiting Yang , Siang Lv , Xin Guan , Bingnan Lu , Yuntao Yao , Runzhi Huang , Yifan Liu , Yanhua Du , Jun Wu

引用次数: 0

High-dose vitamin C: A promising anti-tumor agent, insight from mechanisms, clinical research, and challenges 高剂量维生素C：一种很有前景的抗肿瘤药物，从机制、临床研究和挑战方面的见解

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-06-27 DOI: 10.1016/j.gendis.2025.101742

Hanzheng Zhao , Wentao Fu , Xiaobao Yang , Wenhui Zhang , Si Wu , Jingxin Ma , Tianzhen Zhang , Hongwei Yao , Zhongtao Zhang

Vitamin C, also known as ascorbic acid, has sparked controversy since it first emerged as a potential anti-cancer agent. However, an increasing number of preclinical studies have demonstrated that high-dose vitamin C exhibits selective anti-tumor effects, including “pro-oxidative cytotoxicity”, “anti-cancer epigenetic regulation”, and “immune modulation”. Consequently, vitamin C has reemerged as a promising anti-cancer therapy in the form of high-dose administration. Advancements in pharmacokinetic research have facilitated the development of clinical trials. Early clinical studies across various cancer types have confirmed the safety of high-dose vitamin C administered via intravenous injection. Moreover, its use as an adjuvant therapy in combination with standard treatments, such as chemotherapy and radiotherapy, has shown promising therapeutic potential. However, there remains a lack of consensus regarding optimal dosage, administration methods, tumor specificity, and patient selection. These factors have contributed to the inconsistent outcomes observed in phase II clinical trials and have hindered the widespread conduct of phase III trials. Without robust clinical evidence, high-dose vitamin C, despite being a non-toxic and promising anti-cancer agent, risks being “shelved” once again. In this review, we provide a comprehensive overview of the anti-tumor mechanisms of high-dose vitamin C and a detailed analysis of preclinical and clinical studies investigating its role as an anti-cancer agent. Additionally, we explore emerging trends in high-dose vitamin C therapy for cancer treatment and offer recommendations for future research in this field.

维生素C，也被称为抗坏血酸，自从它第一次作为潜在的抗癌剂出现以来就引发了争议。然而，越来越多的临床前研究表明，高剂量维生素C具有选择性抗肿瘤作用，包括“促氧化细胞毒性”、“抗癌表观遗传调节”和“免疫调节”。因此，维生素C以高剂量给药的形式重新成为一种有前途的抗癌疗法。药代动力学研究的进步促进了临床试验的发展。针对各种癌症类型的早期临床研究已经证实，静脉注射高剂量维生素C是安全的。此外，将其作为辅助治疗与标准治疗（如化疗和放疗）相结合，已显示出良好的治疗潜力。然而，关于最佳剂量、给药方法、肿瘤特异性和患者选择仍然缺乏共识。这些因素导致了II期临床试验中观察到的结果不一致，并阻碍了III期试验的广泛开展。没有强有力的临床证据，大剂量维生素C，尽管是一种无毒的、有希望的抗癌剂，有再次被“搁置”的风险。本文综述了高剂量维生素C的抗肿瘤机制，并对其作为抗癌药物的临床前和临床研究进行了详细分析。此外，我们探讨了高剂量维生素C治疗癌症的新趋势，并为该领域的未来研究提出了建议。

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引用次数: 0

Regulation of de novo lipogenesis and lipophagy by SP1 gene variants SP1基因变异对新生脂肪生成和脂肪吞噬的调控

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-06-27 DOI: 10.1016/j.gendis.2025.101722

Soo Yeon Kim, Hyo-Jeong Ban, Siwoo Lee, Hee-Jeong Jin

引用次数: 0

ROS accelerates the progression of hypertrophic cardiomyopathy 活性氧加速肥厚性心肌病的进展

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-06-27 DOI: 10.1016/j.gendis.2025.101741

Jinhua Cao , Yafei Zhai , Ke Li , Jiajv Li , Xiaoxu Tian , Jianchao Zhang , Shuang Li , Mengduan Liu , Xiaowei Li , Jianzeng Dong , Xiaofang Wang

MYBPC3 mutations are the leading cause of hypertrophic cardiomyopathy. Here, to study the pathogenesis of hypertrophic cardiomyopathy, we created a MYBPC3 knockout (KO) model using human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). MYBPC3-deleted hiPSC-CMs revealed the characteristics of heart failure, which exhibited increased contractility at 30 days but decreased at 40 days. Furthermore, at 40 days, it also shows abnormal calcium handling, increased ROS levels, and mitochondrial damage. Further RNA sequencing revealed that the oxidative stress pathway was aberrant, in addition to alterations linked to hypertrophic cardiomyopathy. Moreover, after adding melatonin to hiPSC-CMs at 30 days, MYBPC3-deleted hiPSC-CMs showed restored calcium handling capacity, decreased ROS levels, and improved myocardial contractility. In summary, reducing ROS can improve the phenotype of hypertrophic cardiomyopathy.

MYBPC3突变是肥厚性心肌病的主要原因。为了研究肥厚性心肌病的发病机制，我们利用人诱导多能干细胞来源的心肌细胞（hiPSC-CMs）建立了MYBPC3基因敲除（KO）模型。mybpc3缺失的hiPSC-CMs显示心力衰竭的特征，30天收缩力增加，40天收缩力下降。此外，在第40天，还表现出钙处理异常，ROS水平升高和线粒体损伤。进一步的RNA测序显示，除了与肥厚性心肌病相关的改变外，氧化应激途径是异常的。此外，在hiPSC-CMs中添加褪黑素30天后，mybpc3缺失的hiPSC-CMs显示钙处理能力恢复，ROS水平降低，心肌收缩力改善。综上所述，减少ROS可以改善肥厚性心肌病的表型。

引用次数: 0

Transcriptional profiling reveals glucose-dependent regulation of COL13A1 mRNA in Pompe patients: Prospect for a novel disease mechanism 转录谱分析揭示了Pompe患者COL13A1 mRNA的葡萄糖依赖性调节：一种新的疾病机制的前景

IF 9.4 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Genes & Diseases

Pub Date : 2025-06-26 DOI: 10.1016/j.gendis.2025.101738

S. Uyttebroeck , D.V. Ngoc , R. Osei , K. Dohr , P. Giron , B.J.H. Dequeker , S. Seneca , K. Sermon , F.J. Hes , A. Gheldof

引用次数: 0

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