Molecular medicine reports最新文献

{"title":"[Expression of Concern] Resveratrol improves neurological outcome and neuroinflammation following spinal cord injury through enhancing autophagy involving the AMPK/mTOR pathway.","authors":"Hong-Yu Meng, De-Cheng Shao, Han Li, Xiao-Dan Huang, Guang Yang, Bing Xu, Hai-Yun Niu","doi":"10.3892/mmr.2025.13679","DOIUrl":"10.3892/mmr.2025.13679","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the confocal microscopic images shown in Fig 3, the top (Sham) and bottom (SCI) data panels appeared to show a small section of overlapping data, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 18: 2237‑2244, 2018; DOI: 10.3892/mmr.2018.9194].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447045/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Corrigendum] Reactive oxygen species‑mediated activation of the Src‑epidermal growth factor receptor‑Akt signaling cascade prevents bortezomib‑induced apoptosis in hepatocellular carcinoma cells.","authors":"Jinlin Hou, Anguo Cui, Peiying Song, Hui Hua, Ting Luo, Yangfu Jiang","doi":"10.3892/mmr.2025.13677","DOIUrl":"10.3892/mmr.2025.13677","url":null,"abstract":"<p><p>Following the publication of the above article, the authors have realized that there were several duplicated western blots featured in Figs. 2‑4. The EGFR blot correctly presented for Fig. 3 (the HepG2 cell line) had been inadvertently featured in Fig. 2 (the EGFR blot for the HepG2 cell line). In Fig. 3, the incorrectly assembled Akt blot for the SMMC‑7721 group was the source image for the correctly presented Akt band in Fig. 1 (the SMMC‑7721 cell line), whereas the Akt blot correctly presented for the Hep3B cell line had been inadvertently featured as the actin blot of the HepG2 cell line. The p‑Src blot correctly presented for Fig. 2 (the SMMC‑7721 cell line) had been inadvertently featured in Fig. 4C (the p‑Src blot for SMMC‑7721). Additionally, the actin blots correctly presented for Fig. 2 (the SMMC‑7721 and HepG2 cell lines) were incorrectly assembled into Fig. 4C (the actin blots for SMMC‑7721 and HepG2). The revised versions of Figs. 2‑4, now showing the correct data for the EGFR blot of the HepG2 cell line in Fig. 2, the Akt blot for the SMMC‑7721 cell line and the actin blot for the HepG2 cell line in Fig. 3, the p‑Src blot for the SMMC‑7721 cell line and the actin blots for SMMC 7721 and HepG2 in Fig. 4C, are shown on the next two pages. The authors wish to state that these errors were made during the figure assembly process, and did not affect either the results or the conclusions reported in this paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of <i>Molecular Medicine Reports</i> for granting them the opportunity to publish this. The authors regret that these errors were included in the paper, and also apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 11: 712‑718, 2015; DOI: 10.3892/mmr.2014.2736].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12446904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145041019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research advancements regarding the relationship between FBXO2 and malignant tumors (Review).","authors":"Jieya Zhang, Jize Yang, Xiaomin Zhang, Yiran Yuan, Shuai Sun, Shihua Zhang, Jiefeng He","doi":"10.3892/mmr.2025.13690","DOIUrl":"10.3892/mmr.2025.13690","url":null,"abstract":"<p><p>The ubiquitin‑proteasome system (UPS) acts as a central regulator for a range of protein components, including ubiquitin, ubiquitin‑activating enzyme (E1), ubiquitin‑conjugating enzyme (E2), ubiquitin ligase (E3), the 26S proteasome and deubiquitinating enzyme. These components function in a coordinated manner to facilitate the repair and degradation of proteins. Among the ubiquitinating enzymes, in conjunction with E1‑activating enzymes and E2‑binding enzymes, it attaches to substrates and promotes the transfer of ubiquitin molecules to target proteins. The S‑phase kinase‑associated protein 1 (SKP1)‑Cullin‑F‑box (SCF) complex is one of the E3 ligases involved in cancer progression, and consists of four primary components: i) SKP1; ii) Cullin 1/coiled‑coil domain containing 53; iii) ring box protein 1/RING‑box 1/RING‑box protein HRT1; and iv) F‑box protein (FBP). Each FBP can recognize and bind to a different set of substrates, which determines the specificity of the targets of the SCF complex. In addition to being components of the SCF complex, FBPs participate in processes such as DNA replication, transcription, cell differentiation and cell death. F‑box protein 2 (FBXO2), a member of the human FBP family, functions as a subunit of FBP ubiquitin ligases and is highly expressed in the cytoplasm of eukaryotic cells. FBXO2 is highly expressed in various malignant tumors, and is closely associated with tumor cell proliferation, migration and invasion. The present review presents the composition of the UPS and FBP families and their roles in malignant tumors, with a focus on advancements in research into the relationships between FBXO2 and various malignant tumors, aiming to acquire a more profound understanding of their potential mechanisms in the development of malignant tumors and to offer novel ideas for tumor therapy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PARP‑1 in liver diseases: Molecular mechanisms, therapeutic potential and emerging clinical applications (Review).","authors":"Kaipeng Hu, Heng Tian, Shuxing Chen, Yuhan Liu, Ran Wei, Bangjie Chen, Yiwen Jia","doi":"10.3892/mmr.2025.13689","DOIUrl":"10.3892/mmr.2025.13689","url":null,"abstract":"<p><p>The liver, despite its capacity for self‑repair, faces major challenges when excessive damage leads to fibrosis and impaired function, potentially progressing to severe liver diseases, including cirrhosis, hepatocellular carcinoma (HCC) and non‑alcoholic fatty liver disease (NAFLD). Although advancements in understanding the molecular landscapes of these conditions have been made, clinical outcomes remain suboptimal. Therefore, novel therapeutic targets are necessary. Poly(ADP‑ribose) polymerase‑1 (PARP‑1), a pivotal enzyme in DNA damage response and repair, has emerged as a critical contributor to liver pathophysiology. The present review explores the expression, regulation and mechanism of action of PARP‑1 in various liver diseases, including viral hepatitis, alcoholic liver disease, NAFLD, hepatic fibrosis, HCC, drug‑induced liver injury and autoimmune liver diseases. The involvement of PARP‑1 in key cellular signaling pathways, particularly those associated with inflammation, apoptosis and immune regulation, highlights its clinical relevance as a biomarker and therapeutic target. The potential of PARP inhibitors to improve outcomes in patients with liver disease is discussed, both as stand‑alone treatments and in combination with modalities such as immune checkpoint inhibitors and DNA damage repair inhibitors. Leveraging recent advancements in PARP imaging and rare genetic biomarker research, this review underscores the potential of PARP‑1‑based diagnostics and therapies while advocating for future studies to overcome resistance mechanisms and expand therapeutic applications.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small dense LDL: An underestimated driver of atherosclerosis (Review).","authors":"Makhabbat Bekbossynova, Timur Saliev, Tatyana Ivanova-Razumova, Saltanat Andossova, Aknur Kali, Gulzhan Myrzakhmetova","doi":"10.3892/mmr.2025.13693","DOIUrl":"https://doi.org/10.3892/mmr.2025.13693","url":null,"abstract":"<p><p>Cardiovascular disease remains the leading cause of death globally, despite advances in lipid‑lowering strategies. A distinct subfraction of low‑density lipoprotein (LDL) particles, known as small LDL (sdLDL; particle size, 15‑20 nm), has been found to play a disproportionately large role in atherogenesis and residual cardiovascular risk when present at elevated concentrations, particularly in individuals with normocholesterolemia but underlying metabolic disorders. The present review critically examines the pathophysiological characteristics that render sdLDL highly atherogenic. These include increased permeability, prolonged circulation and heightened susceptibility to oxidative modification. The review also explores how sdLDL promotes endothelial dysfunction, foam cell formation, inflammation and plaque instability. Furthermore, it emphasizes the diagnostic challenges of sdLDL measurement, its clinical relevance in high‑risk populations and the limitations of current lipid panels in capturing its contribution to disease progression. Elevated sdLDL levels are commonly observed among individuals with metabolic syndrome, insulin resistance, type 2 diabetes and obesity. Multiple epidemiological studies indicate that elevated sdLDL levels are an independent predictor of cardiovascular events. Targeted lifestyle and pharmacological strategies to reduce sdLDL levels are also reviewed, including statins, fibrates, niacin, w‑3 fatty acids, proprotein convertase subtilisin/kexin type 9 inhibitors and RNA‑targeting agents. The greater incorporation of sdLDL testing into risk assessment tools and clinical guidelines is recommended, and strategies for advancing diagnostics, including artificial intelligence‑driven prediction models and advanced lipid profiling are proposed.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atractylodin inhibits ferroptosis in sepsis‑induced acute gastrointestinal injury via SIRT3/PRDX3.","authors":"Yun-Xia Hu, Ming-Qi Chen, Jian-Lin Wang, Tao Wu, Hai-Dong Zhang, Tong-Tong Li, Hui Gao, Yu Bai","doi":"10.3892/mmr.2025.13695","DOIUrl":"https://doi.org/10.3892/mmr.2025.13695","url":null,"abstract":"<p><p>Gastrointestinal injury (GI) is a significant concern in various medical contexts, particularly in patients undergoing antiplatelet therapy, experiencing trauma, or dealing with the effects of medications. The present study investigated the effect of atractylodin, a bioactive compound derived from <i>Atractylodes lancea</i> (Thunb.) DC., traditionally used in medicinal applications. A sepsis animal model was established through cecal ligation and perforation. Mice were treated with atractylodin, with or without silencing of NAD‑dependent protein deacetylase sirtuin‑3 (SIRT3), via transfection with adeno‑associated virus (AAV) vectors. Atractylodin markedly improved mitochondrial function <i>in vivo</i>, as evidenced by increased mitochondrial‑related proteins via western blot analysis (TOM20) and increased mitochondrial membrane potential, as observed via JC‑1 staining. In addition, atractylodin treatment inhibited apoptosis. Together, these changes regulated mitochondrial dysfunction. Moreover, atractylodin improved the prognosis of sepsis‑induced ferroptosis in the stomach and colon tissues. Atractylodin markedly activated SIRT3 while suppressing the expression of ac‑peroxiredoxin‑3 (PRDX3). Notably, the knockdown of SIRT3 diminishes the inhibitory effect of atractylodin on ferroptosis, when AAV‑short hairpinSIRT3 was injected into the stomach and colon tissues of C57 BL/6 mice. Further, atractylodin may have attenuated GI development by preventing mitochondrial dysfunction through the SIRT3/PRDX3 pathway. Hence, protection against mitochondrial dysfunction using atractylodin may be a promising therapeutic strategy against sepsis‑induced acute GI.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] Inhibition of tumorigenesis and invasion of hepatocellular carcinoma by siRNA‑mediated silencing of the <i>livin</i> gene.","authors":"Hui Liu, Shaochuang Wang, Hangyong Sun, Zeya Pan, Weiping Zhou, Mengchao Wu","doi":"10.3892/mmr.2025.13683","DOIUrl":"10.3892/mmr.2025.13683","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, regarding the cell invasion assay data shown in Fig. 4A, the 'Control' and 'pU‑siNC' data panels appeared to share an overlapping section of data, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original source. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper; however, up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 3: 903‑907, 2010; DOI: 10.3892/mmr.2010.355].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12455552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HSPD1 regulates angiotensin II‑induced atrial fibrillation via the PPAR signaling pathway.","authors":"Yimeng Zhou, Lianzhi Zhang, Shunping Zhou, Wenjia Zhang, Qunlin Gong, Nan Xu, Jiahong Wang, Zhong Zhang, Nannan Chen","doi":"10.3892/mmr.2025.13696","DOIUrl":"10.3892/mmr.2025.13696","url":null,"abstract":"<p><p>Atrial fibrillation (AF) is a multifactorial condition, and understanding its molecular mechanisms is key for developing targeted therapies. The present study aimed to investigate the role of heat shock protein D1 (HSPD1) in the pathogenesis of AF, particularly in angiotensin II (Ang II)‑induced cardiac fibroblasts (CFs). Differentially expressed genes (DEGs) were screened from the GSE31821 dataset for enrichment analysis, protein‑protein interaction (PPI) network construction and the hub gene HSPD1 was identified. <i>In vitro</i> experiments, including Cell Counting Kit‑8 and Transwell migration assay, Reverse transcription‑quantitative (RT‑q)PCR, Western blotting and ELISA, were conducted to evaluated the effects of Ang II on CF viability, migration, fibrosis‑associated markers (collagen I, collagen III and α‑smooth muscle actin) and HSPD1 expression. The effects of HSPD1 knockdown on cell viability, inflammatory cytokines (TNF‑α, IL‑8 and IL‑1β), AF‑associated proteins [atrial natriuretic peptide (ANP), β‑major histocompatibility complex (MHC) and MMP‑2] and peroxisome proliferator‑activated receptor (PPAR) signaling pathways were investigated. A total of 582 DEGs were identified, with significant involvement of pathways such as 'MAPK signaling pathway' and 'Wnt signaling pathway'. A total of five genes (HSP90AA1, HSP90AB1, HSPA4, HSPA8 and HSPD1) were highly expressed in AF samples. <i>In vitro</i>, Ang II‑induced fibrotic changes in CFs included increased viability, migration and upregulated fibrosis markers and HSPD1 expression. HSPD1 knockdown decreased Ang II‑induced secretion of inflammatory cytokines (TNF‑α, IL‑8 and IL‑1β) and expression of AF‑associated proteins (ANP, β‑MHC and MMP‑2). Downregulation of PPAR signaling proteins (PPARα, PPARγ, carnitine palmitoyltransferase I and sirtuin3) were observed, while thiazolidinedione treatment partially prevented Ang II‑induced changes. HSPD1 serves a key role in Ang II‑induced CF function, promoting fibrosis, inflammation and AF‑associated protein expression. Targeting HSPD1 in combination with PPAR pathway modulation presents a promising therapeutic strategy for AF treatment.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145150043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNA hsa_circ_0000118 promotes atrial fibrosis by regulating the microRNA‑34a‑5p/Smad4 axis.","authors":"Na Wu, Yuanbo Zhang, Yuhong Zeng, Lanqing Yang, Jun Li, Yanxiu Chen, Zhiquan Yuan, Xinghua Chen, Chengying Li, Long Wu, Tongjian Cai, Zhihui Zhang, Li Zhong, Yafei Li","doi":"10.3892/mmr.2025.13704","DOIUrl":"https://doi.org/10.3892/mmr.2025.13704","url":null,"abstract":"<p><p>The regulatory functions and underlying mechanisms of circular RNAs (circRNAs/circs) in atrial fibrillation (AF) are largely unknown. The present study aimed to assess the prognostic roles and potential biological functions of hsa_circ_0000118 in structural remodeling in AF. Gain‑ and loss‑of‑function cell models were established in mouse cardiac fibroblasts. Cell Counting Kit‑8 and Transwell assays were used to analyze the proliferation and migration of cardiac fibroblasts. To evaluate the underlying mechanisms, RNA immunoprecipitation and luciferase reporter assays were performed. hsa_circ_0000118 was demonstrated to be significantly upregulated in atrial tissues of patients with valvular heart disease with AF compared to those without AF. Elevated plasma levels of hsa_circ_0000118 were independently associated with poor prognosis in patients with AF. <i>In vitro</i>, hsa_circ_0000118 promoted collagen I and collagen III expression, and the migration of cardiac fibroblasts. Functional assays demonstrated that hsa_circ_0000118 acted as a competing endogenous RNA of microRNA (miR)‑34a‑5p to reduce the suppressive effect of miR‑34a‑5p on its target Smad4 in cardiac fibroblasts. In conclusion, hsa_circ_0000118 may serve as a non‑invasive prognostic biomarker for AF. The newly identified roles of hsa_circ_0000118 in AF provide a mechanistic understanding of structural remodeling in AF and pave the way towards novel therapies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of lactylation on the pathogenesis of cancer and its clinical application potential (Review).","authors":"Xiaomei Wang, Jiaqing Chen, Bing Wang, Yanping Li, Xinyue Zhou, Yingqiu Song, Chenggui Miao, Yurong Huang","doi":"10.3892/mmr.2025.13702","DOIUrl":"https://doi.org/10.3892/mmr.2025.13702","url":null,"abstract":"<p><p>Dysregulation of lactate metabolism is a hallmark of multiple pathologies, including cancer, which coordinates metabolic reprogramming and malignant progression. Lactylation, a lactate‑derived post‑translational modification, is a key regulator of tumor cell adaptation, aggressive behavior and immune escape. This modification mechanism links lactate accumulation to carcinogenic signaling and epigenetic dysregulation, providing novel insights into cancer pathogenesis. The present review summarizes the roles of lactylation in tumor microenvironment (TME) remodeling, therapeutic resistance and immunomodulation, and outlines the challenges to clinical translation. Lactate drives the lactylation of histone and non‑histone proteins, and alters chromatin structure and transcriptional programs to maintain tumorigenesis. In the TME, lactylation modulates the phenotypes of stromal cells (such as cancer‑associated fibroblasts) and immune cells (including macrophages and T cells), forming an immunosuppressive niche. Lactylation can also polarize macrophages towards a tumor‑promoting state, inhibit CD8+ T cells and upregulate immune checkpoints. Clinically, lactylation is associated with chemotherapy resistance (such as paclitaxel in breast cancer) and a poor prognosis, highlighting its usefulness as a biomarker. Notably, therapeutic strategies targeting lactate synthesis (such as lactate dehydrogenase A inhibitors), lactate transport (for example, monocarboxylate transporter 1/4 blockers) or lactase (such as histone lactate transferase) have shown promise in preclinical models. In conclusion, lactylation promotes tumor progression while also providing a viable therapeutic target. Deciphering its environment‑dependent mechanisms, particularly its interactions with immune checkpoints and metabolic vulnerabilities, may advance precision oncology. Validating biomarkers and therapies centered on lactylation is a key frontier in improving clinical outcomes.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 6","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}