{"title":"Potential regulatory role of the m <sup>6</sup>A-lncRNA axis in breast cancer: molecular mechanisms and therapeutic implications.","authors":"Di Chen, Jinyan Wang, Xichun Hu, Shu Liu","doi":"10.3724/abbs.2025134","DOIUrl":"https://doi.org/10.3724/abbs.2025134","url":null,"abstract":"<p><p>N6-methyladenosine (m <sup>6</sup>A) modification, the most prevalent internal modification in eukaryotic messenger RNAs (mRNAs), has emerged as a crucial regulator of various biological processes. This reversible epigenetic modification is dynamically regulated by methyltransferases (writers), demethylases (erasers), and m <sup>6</sup>A-binding proteins (readers). Aberrant m <sup>6</sup>A modification is associated with the initiation, progression, and metastasis of breast cancer, highlighting its potential as a therapeutic target. Long non-coding RNAs (lncRNAs), a class of non-protein-coding transcripts longer than 200 nucleotides, are also involved in breast cancer development through diverse mechanisms. Increasing evidence suggests a complex interplay between m <sup>6</sup>A modifications and lncRNAs in breast cancer, with lncRNAs modulating m <sup>6</sup>A regulators and m <sup>6</sup>A-modified lncRNAs exerting functional effects. This review comprehensively summarizes the current understanding of the m <sup>6</sup>A-lncRNA axis in breast cancer, including the molecular mechanisms underlying its interaction and its effects on breast cancer biological processes, such as proliferation, apoptosis, migration, invasion, and therapy resistance, and highlights the potential of this axis as a diagnostic and therapeutic biomarker. Additionally, we discuss the challenges and future directions in this rapidly evolving field, aiming to provide insights for the development of novel therapeutic strategies for breast cancer.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The expression profile of type 1 equilibrative nucleoside transporter in aged C57BL/6J mouse brain.","authors":"Xiao-Yuan Zhang, Ziteng Ma, Ya-Han Jin, Zhimin Long, Qing Tang, Guiqiong He, Yun-Fang Jia","doi":"10.3724/abbs.2025127","DOIUrl":"https://doi.org/10.3724/abbs.2025127","url":null,"abstract":"<p><p>The type 1 equilibrative nucleoside transporter (ENT1) is essential for regulating extracellular adenosine levels and has been implicated in various psychiatric disorders. While previous studies have investigated the expression of ENT1 in fetal and neonatal brains, its neuroanatomical distribution in adult and aged mouse brains has not been fully elucidated. Therefore, in this study, we utilize immunohistochemistry and double-immunofluorescence techniques to map the expression of ENT1 across various brain regions. Our findings demonstrate that ENT1-positive cells are widely distributed throughout the brain, with particularly high expression observed in the cerebral cortex and hippocampus. ENT1 is expressed predominantly in neurons, particularly in cholinergic, dopaminergic and glutamatergic neurons. Furthermore, ENT1 is localized primarily to the mitochondria and lysosomes and is expressed to a lesser extent in the Golgi apparatus and endoplasmic reticulum. Notably, we find an age-dependent increase in ENT1 expression in the cerebral cortex, suggesting a potential role in age-related cognitive functions. This study highlights the regionally specific expression of ENT1 in the brain, providing a new morphological basis for understanding its potential roles in brain physiology. Additionally, given its involvement in neurotransmitter regulation, ENT1 may have important implications for neurological and psychiatric disorders. This work lays the groundwork for future studies exploring the implications of ENT1 in neurodegenerative diseases and other aging-related brain disorders.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144726424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rongjuan Wei, Tao Zhong, Ke Deng, Xianglong Zhang, Dongping Li, Meiling Chen, Ping Chang, Peng Wu, Zhanguo Liu
{"title":"Rhamnose alleviates the proinflammatory response during endotoxemia via the CEACAM1/LGALS9-p38 axis.","authors":"Rongjuan Wei, Tao Zhong, Ke Deng, Xianglong Zhang, Dongping Li, Meiling Chen, Ping Chang, Peng Wu, Zhanguo Liu","doi":"10.3724/abbs.2025109","DOIUrl":"https://doi.org/10.3724/abbs.2025109","url":null,"abstract":"<p><p>Gut microbiota plays an important role in orchestrating the host immune response. We previously reported that gut microbiota-derived rhamnose enhances the phagocytosis of macrophages, upon which we further asked whether rhamnose has modulatory effects on inflammation. Here, we show that, in an LPS-induced endotoxic mouse model, plasma rhamnose levels are increased. This bacteria-derived sugar alone does not impact inflammatory cytokine homeostasis or cause organ damage. In contrast, it is able to alleviate endotoxin-induced systemic inflammation and organ damage. Mechanistically, in macrophages <i>in vitro</i>, rhamnose binds to the V39, D40, and T101 sites of carcinoembryonic antigen-associated cell adhesion molecule 1 (CEACAM1), subsequently promoting the interaction between CEACAM1 and galectin 9 (LGALS9), which increases the protein level of dual-specificity protein phosphatase 1 (DUSP1). This inhibits p38 phosphorylation and thus attenuates the LPS-triggered expressions of proinflammatory factors. Collectively, our results suggest that rhamnose signals via the CEACAM1/LGALS9-p38 axis, which suppresses endotoxemia-associated inflammation, and that rhamnose is a candidate anti-inflammatory agent for the control of infection-induced organ damage.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144705958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chulan Yang, Hongyu Zhao, Jing Tuo, Wei Zhao, Zhiwei Zhang, Zemin Pan, Lianghai Wang, Haixuan Zhao, Songhua Zhao, Hongtao Li
{"title":"Zinc finger protein 154 inhibits the growth and metastasis of cervical cancer cells through inhibiting Wnt/β-catenin signaling by upregulating NLK.","authors":"Chulan Yang, Hongyu Zhao, Jing Tuo, Wei Zhao, Zhiwei Zhang, Zemin Pan, Lianghai Wang, Haixuan Zhao, Songhua Zhao, Hongtao Li","doi":"10.3724/abbs.2025118","DOIUrl":"https://doi.org/10.3724/abbs.2025118","url":null,"abstract":"","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144697315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Langlin Ou, Zitong Meng, Jian Mei, Hao Yuan, Xiangrui Zhu, Xiaoying Wang, Ao Shen, Zhaosi Wang, Lixin Zhang, Song Wang, Yingli Chen, Xiangming Pang, Yuxiang Liu, Yadong Xu, Cui Ma
{"title":"LPS mediates cuproptosis and inflammation in THP-1 macrophages through HKDC1.","authors":"Langlin Ou, Zitong Meng, Jian Mei, Hao Yuan, Xiangrui Zhu, Xiaoying Wang, Ao Shen, Zhaosi Wang, Lixin Zhang, Song Wang, Yingli Chen, Xiangming Pang, Yuxiang Liu, Yadong Xu, Cui Ma","doi":"10.3724/abbs.2025089","DOIUrl":"https://doi.org/10.3724/abbs.2025089","url":null,"abstract":"<p><p>Cuproptosis is a recently identified form of copper-driven cell death characterized by the aggregation of acylated proteins and proteotoxic stress in the mitochondrial tricarboxylic acid cycle, which plays a role in inflammation. Recent studies suggest that hexokinase structural domain protein 1 (HKDC1), a fifth hexokinase, is involved in regulating mitochondrial function. However, the role of HKDC1 in cuproptosis and LPS-induced macrophage inflammation remains unclear. Here, we assess macrophage plasticity using CCK8 viability assays and phagocytosis activity experiments in an <i>in vitro</i> inflammatory model of THP-1 cells. We measure the levels of inflammatory factors and cuproptosis-related proteins using western blot analysis and RT-qPCR. Additionally, we examine the expression and localization of the HKDC1 protein using ChIP-qPCR and immunofluorescence staining. We find that LPS promotes the expressions of inflammatory factors and decreases cuproptosis levels in THP-1-derived macrophages while also activating glycolysis and inducing the expression of HKDC1 via the Toll-like receptor 4 (TLR4) receptor. We further demonstrate that <i>HKDC1</i> knockdown inhibits glycolysis and induces cuproptosis. Mechanistically, we provide the first evidence that LPS promotes the binding of Yin Yang 1 (YY1) to the <i>HKDC1</i> promoter, thereby regulating <i>HKDC1</i> transcription. HKDC1 interacts with heat shock cognate B (HSCB) and ferredoxin 1 (FDX1), leading to increased intracellular copper levels and subsequent cuproptosis. <i>HKDC1</i> knockdown <i>in vivo</i> alleviates acute sepsis by activating copper-dependent cell death pathways. Collectively, our findings suggest that LPS mitigates cuproptosis and promotes inflammation via HKDC1, suggesting a new cuproptosis-dependent anti-inflammatory strategy.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144681784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yiyao Liang, Minyan Wei, Yunan Yao, Baizhong Chen, Jinji Deng, Shiqi Xu, Liming Li, Wen Liu, Yi Cai, Guodong Zheng
{"title":"Nobiletin suppresses nasopharyngeal carcinoma by regulating the KEAP1/NRF2/ARE pathway.","authors":"Yiyao Liang, Minyan Wei, Yunan Yao, Baizhong Chen, Jinji Deng, Shiqi Xu, Liming Li, Wen Liu, Yi Cai, Guodong Zheng","doi":"10.3724/abbs.2025113","DOIUrl":"https://doi.org/10.3724/abbs.2025113","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC) ranks among the most prevalent malignancies, particularly in East Asia and Southeast Asia. Nobiletin (NOB), an exclusive polymethoxyflavonoid derived from citrus peel, exhibits diverse physiological properties, notably its potent anticancer activity. Kelch-like ECH-associated protein 1 (KEAP1), the repressor protein regulating the nuclear factor erythroid 2-related factor 2 (NRF2) transcription factor, has emerged as a promising strategy for addressing oxidative stress in various diseases. The KEAP1/NRF2/ARE signal is a fundamental pathway within the cellular homeostatic defense system. This study robustly demonstrates the chemopreventive potential of NOB through comprehensive <i>in vitro</i> and <i>in vivo</i> assessments using subcutaneous tumor mouse models. Furthermore, our groundbreaking findings reveal that NOB effectively hinders the migration and invasion capacities of CNE-2 and 5-8F (NPC) cells in a dose- and time-dependent manner. Mechanistically, NOB, a potent KEAP1 activator, significantly disrupts the NRF2/ARE signaling pathway by accelerating the proteasomal degradation of NRF2 and suppressing its nuclear translocation. Consequently, this cascade reduces the expressions of ARE-driven genes and antioxidant enzymes, thereby increasing intracellular reactive oxygen species (ROS) levels and increasing antitumor immunity. Moreover, the sensitivity induced by NOB is markedly diminished in CNE-2 cells following the gene silencing of <i>KEAP1</i>. These findings underscore the pivotal role of NOB in activating KEAP1. Overall, KEAP1 has emerged as a compelling target for potential malignancy treatment in nasopharyngeal carcinoma cell lines. Our results suggest the promising application of NOB as a natural sensitizer in chemotherapy, opening avenues for promising therapeutic interventions.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144681785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chunyan Li, Wuzheng Liu, Yana Xiao, Tenglong Dai, Yu Su, Yubin Wang, Ao Zhang, Ruichen Liu, Xianglong Zhao, Zhao Zhang, Shangqi Yin, Jun Wu
{"title":"Quantitative liquid chromatography-tandem mass spectrometric analysis of 11dH-TXB2 and creatinine in urine.","authors":"Chunyan Li, Wuzheng Liu, Yana Xiao, Tenglong Dai, Yu Su, Yubin Wang, Ao Zhang, Ruichen Liu, Xianglong Zhao, Zhao Zhang, Shangqi Yin, Jun Wu","doi":"10.3724/abbs.2025055","DOIUrl":"https://doi.org/10.3724/abbs.2025055","url":null,"abstract":"","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aihua Yang, Yuhang Wang, Yifeng Zhang, Xiaojun Wang, Yi Qian, Wenjing Zhao, Hongyan Qian, Jun Ren, Weizhong Zhu
{"title":"Mitochondria-resident SBK3 confers protection against pressure overload-induced heart failure in mice.","authors":"Aihua Yang, Yuhang Wang, Yifeng Zhang, Xiaojun Wang, Yi Qian, Wenjing Zhao, Hongyan Qian, Jun Ren, Weizhong Zhu","doi":"10.3724/abbs.2025098","DOIUrl":"https://doi.org/10.3724/abbs.2025098","url":null,"abstract":"<p><p>Pathological myocardial hypertrophy, often caused by hypertension, is a well-established independent risk factor for heart failure. <i>SBK3</i>, a gene selectively expressed at relatively high levels in cardiac tissues, has an unclear functional role in the heart. This study is designed to examine the role of SBK3 in transverse aortic constriction (TAC)-induced heart failure, aiming to identify a novel mitochondrion-targeted therapeutic strategy for heart failure. The subcellular localization of SBK3 in adult rat cardiomyocytes is investigated by western blot analysis and immunofluorescence staining, which reveal that SBK3 is located in the mitochondria. Subsequent western blot analysis shows that SBK3 protein expression is downregulated under pathological hypertrophy. To assess the functional relevance of this observation, SBK3 is overexpressed both <i>in vivo</i> (via cardiac-specific AAV9-cTNT) and <i>in vitro</i> (via adenoviral transduction). <i>In vitro</i>, adenovirus-mediated overexpression of SBK3 significantly inhibits ANP and BNP expression and increases the Ca <sup>2+</sup> transient amplitude in angiotensin II (Ang II)-induced hypertrophic cardiomyocytes. <i>In vivo</i>, cardiac-specific SBK3 overexpression using cTNT promoter-containing adeno-associated virus 9 inhibits TAC-induced cardiac hypertrophy and heart failure. Mechanistically, SBK3 exerts its cardioprotective effects by preserving the mitochondrial ultrastructure and regulating the balance of respiratory chain complexes. In addition, SBK3 modulates key regulators of mitochondrial dynamics, including fission and fusion proteins, thereby contributing to mitochondrial integrity and protection against pathological cardiac remodeling.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}