Acta biochimica et biophysica Sinica最新文献

{"title":"miR2916-p5 and miR6478 from <i>Forsythia suspensa</i> fruit suppress inflammatory responses by targeting AKT signaling in human colorectal epithelial cells.","authors":"Dan Bai, Md Nur Islam, Dongwan Cheng, Han Feng, Tao Xu","doi":"10.3724/abbs.2026004","DOIUrl":"10.3724/abbs.2026004","url":null,"abstract":"<p><p>Cross-kingdom regulation by microRNAs (miRNAs) has been widely observed across species. Plant-derived miRNAs can be absorbed through the mammalian gastrointestinal tract, subsequently enter the bloodstream, and reach various target tissues. However, the specific composition, types, and functions of miRNAs in traditional Chinese medicinal herbs, such as <i>Forsythia suspensa</i>, remain unexplored. In this study, we identify 225 conserved miRNAs and 121 novel miRNAs in <i>F</i>. <i>suspensa</i> fruit by high-throughput sequencing. Target gene prediction of abundant <i>Forsythia</i>-derived miRNAs reveals that multiple downstream targets of fsu-miR2916-p5 and fsu-miR6478 are components of the human PI3K/AKT pathway, suggesting this pathway may serve as a key regulatory axis co-modulated by <i>Forsythia</i>-derived miRNAs. Overexpression of fsu-miR2916-p5 and fsu-miR6478 in human colorectal epithelial cells DLD1 suppresses the expression of AKT1 and AKT3, as well as the levels of phosphorylated AKT (p-AKT), as demonstrated by western blot analysis. Furthermore, RNA sequencing reveals downregulation of pro-inflammatory genes. RT-qPCR confirms the presence of <i>Forsythia</i>-derived miRNAs in the mouse colon after oral administration of <i>F</i>. <i>suspensa</i> extract, and confocal microscopy analysis validates their accumulation in colonic cells following gavage of synthetic <i>Forsythia</i>-derived miRNAs. Moreover, uptake of synthetic fsu-miR2916-p5 and fsu-miR6478 in DLD1 cells attenuates LPS-induced mitochondrial reactive oxygen species (ROS) production and reduces the expression of inflammation-associated molecules, including ICAM1, TGFBR1, and IL1R1, as assessed by immunofluorescence and western blot analysis. These findings identify miRNAs in <i>F</i>. <i>suspensa</i> and elucidate their regulatory influence on human gene expression and anti-inflammatory activity, thus offering a novel perspective on miRNA-mediated, plant-based therapeutic strategies for colitis.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147519586","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":"Genetic mutation and dysfunction of AT2 cells drive B(a)P/LPS-induced inflammation-related lung tumorigenesis: evidence and mechanism of autophagy.","authors":"Zhihao Tang, Xianchao Zhou, Pingping Shang, Quanping Yan, Ping Lu, Yanting Lei, Chenfeng Hua, Xiaoshan Zhou, Qiao Zhang, Wei Wang, Huaiyong Chen, Jian He, Feifei Feng","doi":"10.3724/abbs.2025238","DOIUrl":"https://doi.org/10.3724/abbs.2025238","url":null,"abstract":"<p><p>The environmental pollutant benzo(a)pyrene (B(a)P), a representative polycyclic aromatic hydrocarbon (PAH), is a recognized carcinogen, and chronic pulmonary inflammation is closely associated with lung carcinogenesis. Although alveolar type 2 (AT2) cells are the origin of lung adenocarcinoma, the genetic and functional changes in AT2 cells and the mechanisms involved in inflammation-related lung tumorigenesis have not been elucidated. Here, C57BL/6J mice are exposed to B(a)P and the inflammatory irritant lipopolysaccharide (LPS) to establish a model of inflammation-related lung tumorigenesis. Single-cell RNA sequencing is performed on lung tissues. DNA mutations in AT2 cells are analyzed via whole-exome sequencing. The protein expression of AT2 cells in lung cancer tissue is determined by immunofluorescence staining. The results reveal that LPS promotes B(a)P-induced lung tumorigenesis; in the whole lungs of B(a)P/LPS, a decreased proportion, altered differentiation trajectory, and increased gene mutation number in AT2 cells are observed. Additionally, in B(a)P/LPS-treated lung cancer tissue, the levels of γ-H2AX DNA damage and the proliferation marker Ki67 in AT2 cells are increased, whereas the levels of differentiation markers are decreased. Single-cell RNA transcriptomics reveals that the autophagy-related genes Foxo3 and Ppp2r5, which are enriched in the PI3K-Akt pathway, and the autophagy-related genes in AT2 cells in lung cancer are decreased in the B(a)P/LPS group. Thus, chronic inflammation promotes DNA damage, gene mutation and dysfunction in AT2 cells, and decreased autophagy in AT2 cells may be an important mechanism for inflammation-related lung tumorigenesis.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147637608","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":"Atractylenolide I mitigates Alzheimer's disease pathology in ApoE ^-/- mice via ARG1/nNOS axis and lipid homeostasis regulation.","authors":"Xun Zhou, Rui Wang, Jingsi Yan, Xiaolang Wu, Dongsheng Yuan, Qi Wang, Huilin Li, Wei Zhao","doi":"10.3724/abbs.2026055","DOIUrl":"https://doi.org/10.3724/abbs.2026055","url":null,"abstract":"<p><p>Apolipoprotein E (ApoE) serves as a critical molecular nexus between Alzheimer's disease (AD) and atherosclerosis, two age-associated inflammatory disorders that share vascular pathology, amyloid-beta (Aβ) deposition, and lipid dysregulation. Atractylenolide I (AI), a promising therapeutic candidate derived from <i>Atractylodes macrocephala</i>Koidz., exhibits multimodal bioactivities with demonstrated anti-inflammatory and neuroprotective properties. To explore its therapeutic potential against AD pathology, we use high-fat diet (HFD)-fed <i>ApoE</i> knockout (ApoE ^-/-) mice treated with or without AI for 12 weeks. Integrated bioinformatics analyses and experimental validation reveal that AI treatment markedly attenuates systemic lipid dyshomeostasis, particularly cerebral lipid deposition, suppresses neuroinflammation via downregulation of M1 macrophage polarization markers, and restores cognitive function through neuronal preservation in hippocampal regions. Mechanistically, AI orchestrates cholesterol efflux by upregulating ATP-binding cassette transporter A1 (ABCA1) and liver X receptor (LXR) expression, while concurrently modulating the abundance of arginine biosynthesis metabolites (urea, malic acid, and creatinine) to rebalance neurovascular homeostasis. Notably, western blot and RT-qPCR analyses reveal that AI differentially regulates key enzymes including arginase 1 (ARG1) and simultaneously upregulates the expression of neuronal nitric oxide synthase (nNOS). Further molecular docking and surface plasmon resonance (SPR) analyses confirm the direct binding of AI to ARG1, indicating a novel neuroprotective mechanism involving the modulation of arginine metabolism. These findings delineate the pleiotropic effects of AI against AD pathology and establish a preclinical foundation for the development of AI-based therapeutics targeting neurodegenerative-cardiovascular comorbidities.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147508626","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":"Discovery and validation of biomarkers for Epstein-Barr virus associated gastric cancer.","authors":"Pincang Xia, Yingying Yu, Xiaoting Xu, Jiajun Lin, Jiayi Shen, Xinyi Lin, Tao Zhang, Zhaowei Xu, Xian-E Peng, Xu Lin","doi":"10.3724/abbs.2026046","DOIUrl":"https://doi.org/10.3724/abbs.2026046","url":null,"abstract":"<p><p>Epstein-Barr virus-associated gastric cancer (EBVaGC) displays unique clinicopathological hallmarks, yet serology-based tools for its detection are still limited. Here, we develop a functional EBV proteome microarray covering 72 viral proteins and apply it to profile antibody responses in 62 gastric cancer patients. The resulting landscape reveals an IgG-skewed humoral signature specific to EBVaGC and identifies 34 EBV antigens exhibiting differential reactivities. Multivariable logistic regression integrates complementary markers into an optimal five-analyte panel (LF2_IgG, BBLF2_IgG, BLRF2_IgG, BPLF1-2_IgA, and BGLF4_IgA) that achieves outstanding discrimination performance (AUC = 0.93) in an independent validation set ( <i>n</i> = 316). The panel's performance is further validated in a community-based screening cohort ( <i>n</i> = 474), where it achieves 87.3% sensitivity and 88.3% specificity for distinguishing EBVaGC from non-malignant gastric conditions spanning gastritis to dysplasia (AUC = 0.94). Together, these results establish a serological framework for EBVaGC diagnosis and provide a scalable strategy for population-level screening that could materially improve the management of this virus-driven malignancy.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147508618","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":"Structural and functional insights into the distinct DNA recognition mechanisms of the terminase small subunit TerS from cyanophages.","authors":"De-Qin Dong, Feng Yang, Kang Du, Kang Xu, Wen-Bin Cheng, Yuxing Chen, Cong-Zhao Zhou, Yong-Liang Jiang","doi":"10.3724/abbs.2026042","DOIUrl":"https://doi.org/10.3724/abbs.2026042","url":null,"abstract":"<p><p>Efficient genome packaging is a critical step in the phage life cycle, directly influencing the viral maturation and infectivity. In tailed phages, this process is driven by a packaging motor composed of a portal protein and a terminase complex. The terminase complex usually consists of a large subunit (TerL) and a small subunit (TerS), which cooperate to recognize, cleave, and translocate genomic DNA into the capsid. However, due to the remarkable diversity and complexity of phage packaging systems, the molecular mechanisms governing TerS-mediated DNA recognition remain poorly understood. Here, we report the 3.51 Å cryo-electron microscopy structure of the TerS from the short-tailed cyanophage Pam5, which infects the host <i>Pseudanabaena mucicola</i> Chao 1806. Pam5 TerS assembles into a nonameric ring with a radially symmetric spiral architecture. Biochemical assays show that Pam5 TerS recognizes the genomic DNA via a specific interaction between the N-terminal helix-turn-helix (HTH) domain of TerS and a 21-bp DNA sequence within the <i>terS</i> gene. In contrast, the TerS from another short-tailed cyanophage, Pam1, which infects the same host, binds to DNA in a sequence-independent manner. These findings reveal that cyanophages, even infecting the same host, could adopt two distinct DNA recognition strategies: HTH-mediated sequence-dependent or sequence-independent modes. This work provides structural and mechanistic insights into the diverse DNA-recognition strategies of TerS and advances our understanding of the evolutionary plasticity of viral genome packaging mechanisms.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493558","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":"PHB2 acts as a braker of progressive pulmonary fibrosis via intervention of DDR2-elicited signaling.","authors":"Penghui Yang, Jinjun Jiang, Jiani Liu, Bing Su, Xiaohua Wang, Zhenli Fu, Ying He, Jing Han, Chunrong Ju, Yinuo Wang, Xinpeng Lu, Xiaomin Peng, Hang Yin, Junqi Li, Dandan Wang, Jianping Liu, Yunxin Lai, Jin Su","doi":"10.3724/abbs.2026009","DOIUrl":"https://doi.org/10.3724/abbs.2026009","url":null,"abstract":"<p><p><p indent=\"0mm\">Idiopathic pulmonary fibrosis (IPF) is a fatal disease whose pathogenic mechanisms remain incompletely understood. Transforming growth factor-beta (TGF-β) is widely regarded as a central driver of fibrosis, orchestrating sustained fibroblast activation and pathological tissue scarring. DDR2 (discoidin domain receptor tyrosine kinase 2), a discoidin domain receptor tyrosine kinase, serves as a critical mediator of non-canonical TGF-β1 signaling. Using lung samples from patients with IPF, human precision-cut lung slices (PCLS), primary lung fibroblasts and a BLM (bleomycin)-induced mouse model, we investigate the role of prohibitin 2 (PHB2) in fibrotic progression. Here, we demonstrate that PHB2 binds to DDR2 and suppresses collagen I-induced DDR2 tyrosine phosphorylation, as well as TGF-β1-stimulated activation of ERK, p38, AKT and Smad-3, leading to downregulation of key fibrotic markers. Accordingly, AAV9-mediated PHB2 overexpression exhibits therapeutic effects in a mouse model of pulmonary fibrosis. We also observe significant downregulation of PHB2 in IPF lungs. Functionally, PHB2 attenuates fibroblast migration and counteracts the TGF-β1-induced enhancement of mitochondrial respiration in lung fibroblasts. Mechanistically, PHB2 disrupts the interaction between DDR2 and TGF-β receptor II (TGFBR2) and inhibits DDR2 phosphorylation, thereby mitigating fibrotic responses in fibroblasts and PCLS- and BLM-induced mouse models. Our findings indicate that PHB2 acts as a molecular \"braker\" of both TGF-β1- and DDR2-driven profibrotic pathways in pathogenic fibroblasts.</p>.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472347","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":"Novel small-molecule positive allosteric modulator 1 with blood-brain barrier penetration activity exerts anti-cellular senescence effects via the PAC1-R/YY1/SIRT6 pathway.","authors":"Wanlin Su, Lin Xiao, Suxiang Tang, Xiaojing Zheng, Yu Zhang, Rongjie Yu","doi":"10.3724/abbs.2026032","DOIUrl":"https://doi.org/10.3724/abbs.2026032","url":null,"abstract":"<p><p><p indent=\"0mm\">Aging is the primary risk factor for neurodegeneration. SIRT6, a key longevity regulator, is downregulated in aged brain tissue and linked to neurodegeneration. Thus, activating SIRT6 may delay brain aging. Based on this, the present study reveals the molecular mechanism by which the novel small-molecule positive allosteric modulator (SPAM1) antagonizes neuronal senescence through the PAC1-R/YY1/SIRT6 signaling axis, along with its highly efficient brain-targeting properties. In a naturally aging model of long-term cultured retinal ganglion cells (RGC-5), sustained administration of SPAM1 <sc>(1 μM)</sc> significantly ameliorates aging phenotypes, including upregulation of SIRT6 and Lamin B1 expressions and suppression of p16 accumulation. Dual luciferase reporter assays confirm that SPAM1 activates the <italic>SIRT6</italic> promoter. Mechanistically, SPAM1 induces nuclear translocation of PAC1-R and releases its 24-kDa C-terminal fragment, which forms a complex with the transcription factor YY1 within the nucleus. ChIP-qPCR confirms that SPAM1 enhances YY1 enrichment on the <italic>SIRT6</italic> promoter, while <italic> YY1</italic> knockdown inhibits SPAM1-mediated SIRT6 activation, establishing YY1's pivotal role. Pharmacokinetics and <italic>in vivo</italic> imaging demonstrate that SPAM1 possesses rapid and persistent brain targeting capabilities: the drug is detectable in the brain within <sc>10 min</sc> after intraperitoneal injection; following tail vein administration, brain fluorescence signals appear within <sc>10 min,</sc> peak at <sc>1 h,</sc> and persist for over <sc>12 h.</sc> This study elucidates SPAM1's anti-neurogerontogenic mechanism through a complete signaling cascade: inducing PAC1-R nuclear translocation, recruiting YY1, and activating SIRT6 transcription. Its well-defined mechanism and unique brain targeting establish a pharmacological foundation for developing innovative drugs to intervene in age-related central nervous system decline.</p>.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147490550","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":"CTCF/STK38 axis drives tumor progression via the Wnt/β-catenin and Hippo pathways.","authors":"Qing Cao, Fangfang Yang, Ye Tian, Qiqi Yang, Lichao Cao, Min Zhao, Yuxin Ren, Xinru Yu, Mengmeng Lai, Yingchun Li, Ming Chen, Jin Yang, Erfei Chen","doi":"10.3724/abbs.2026038","DOIUrl":"https://doi.org/10.3724/abbs.2026038","url":null,"abstract":"<p><p>Metastasis remains the primary driver of cancer-related mortality; therefore, deeper mechanistic insights are needed to develop effective therapeutic strategies. Cutaneous melanoma (SKCM), the most aggressive skin malignancy with increasing incidence worldwide, exemplifies this clinical challenge. Through multiomics analysis of melanoma datasets, we identify serine/threonine kinase 38 (STK38) as a critical mediator of tumor metastasis. Elevated STK38 expression correlates strongly with metastatic progression and reduced survival in melanoma patients. Functional studies demonstrate that STK38 not only regulates cell proliferation and autophagy but also drives migration and epithelial-mesenchymal transition by sensitizing melanoma cells to tumor microenvironmental cues. Transcriptomic profiling reveals that STK38 drives tumor metastasis via the Wnt/β-catenin and Hippo signaling pathways. Mechanistically, ChIP-seq data show that CCCTC-binding factor (CTCF) binds to both the promoter and the first-intron enhancer of <i>STK38</i>. Disruption of these <i>CTCF</i> binding sites via the CRISPR/Cas9 system abolishes chromatin loop formation, suppresses promoter-enhancer functional connectivity, and downregulates STK38 expression. Our findings identify STK38 as a metastasis-promoting regulator in melanoma and suggest that its therapeutic targeting impedes metastatic dissemination.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442152","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":"Natural product 2-dihydroailanthone suppresses colorectal cancer via targeting integrin α3.","authors":"Yunjie Hu, Congcong Li, Yongjiang Wang, Wei Wang, Li Huang, Haoran Lei, Sijuan Sun, Lilian Zhao, Yuanping Liu, Yuting Mu, Zhuohong Li, Hongbin Cheng, Yucheng Gu, Shengxiong Huang, Dong Wang, Dale Guo, Yun Deng","doi":"10.3724/abbs.2026045","DOIUrl":"https://doi.org/10.3724/abbs.2026045","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, necessitating the discovery of novel therapeutic agents. Here, we report a natural small molecule, 2-dihydroailanthone (2-DAIL), as a promising candidate for CRC treatment. First, our results demonstrate that 2-DAIL exhibits significant anti-CRC activity <i>in vitro</i> and <i>in vivo</i>. Then, we find that 2-DAIL directly binds to integrin alpha-3 (ITGA3) revealed by stable isotope labeling by amino acids in cell culture coupled with thermal proteome profiling (SILAC-TPP). Additionally, the RNA sequencing data obtained from CRC cells and tumor tissues suggest that 2-DAIL blocks the PI3K/AKT signaling pathway mediated by ITGA3 inhibition. Collectively, 2-DAIL exerts its anti-CRC effects, at least partially, by binding to and inhibiting the function of ITGA3, thereby blocking the activation of the PI3K/AKT signaling pathway, which leads to CRC cell growth inhibition. Our study provides a promising drug candidate for the treatment of CRC and suggests the potential of 2-DAIL in treating other diseases linked to ITGA3 dysfunction.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442070","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":"ATP-citrate lyase: carcinogenesis and therapeutic advances.","authors":"Liting Meng, Yuru Wang, Qijun Cai, Yang Xi, Desen Sun, Mingxiao Zhao, Qiang Chen","doi":"10.3724/abbs.2026028","DOIUrl":"https://doi.org/10.3724/abbs.2026028","url":null,"abstract":"<p><p>ATP citrate lyase (ACLY) is involved in acetyl-coenzyme A synthesis and protein acetylation, thereby increasing lipid metabolism and altering protein metabolism to affect cellular metabolism. Additionally, ACLY is associated with various biological and pathological functions, especially regarding tumorigenesis. It facilitates the progression of various cancer types, including liver, lung, breast, prostate, and colorectal cancers. Mechanisms underlying ACLY-mediated carcinogenesis are under investigation and may not be limited to energy metabolism and biosynthesis. Acetylation modification of specific signaling molecules and transcription factors is considered a potential mechanism of ACLY-mediated tumorigenesis and offers novel insights and potential targets for the clinical treatment of tumors. Furthermore, the antitumor effect of pharmacological ACLY-inhibiting agents, including various small molecules or naturally active compounds, has been reported, albeit their practical application in clinical settings remains limited. This study aims to comprehensively review the oncogenic role of ACLY, with a focus on major collaborators and regulatory genes.</p>","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147442096","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}