Molecular and Cellular Biochemistry最新文献

{"title":"STAT1 increases the sensitivity of lung adenocarcinoma to carbon ion irradiation via HO-1-mediated ferroptosis.","authors":"Yanliang Chen, Dandan Wang, Hongtao Luo, Mingyu Tan, Qian Wang, Xun Wu, Tianqi Du, Qiuning Zhang, Wenzhen Yuan","doi":"10.1007/s11010-025-05240-z","DOIUrl":"10.1007/s11010-025-05240-z","url":null,"abstract":"<p><p>Radiotherapy is a vital treatment agent for lung adenocarcinoma (LUAD) patients, while radioresistance remains a major factor in treatment failure. Here, we aimed to elucidate how signal transducer and activator of transcription 1 (STAT1) affected sensitivity to carbon ion irradiation for LUAD cells in vivo and in vitro. The results of colony formation, CCK-8, EdU, and calcein-AM/PI double-staining assays demonstrated that the overexpression of STAT1 markedly enhanced the inhibitory effect of carbon ion irradiation on the viability of LUAD cells (A549 and PC9 cells). Lactate dehydrogenase (LDH) leakage assays identified ferroptosis as the predominant form of cell death induced by STAT1 overexpression in LUAD cells. Meanwhile, the ferroptosis-related PCR array confirmed heme oxygenase 1 (HO-1) as a potential effector molecule of STAT1-induced ferroptosis. Mechanistically, STAT1 overexpression resulted in phosphorylation at the serine 727 residue, triggering the upregulation of HO-1 expression and subsequent labile iron pool (LIP) accumulation. This process amplified the Fenton reaction, leading to increased reactive oxygen species (ROS), lipid peroxides (LPO), and glutathione (GSH) depletion. HO-1 knockdown eliminated the ferroptosis induced by the overexpression of STAT1. Furthermore, in vivo experiments showed that STAT1 overexpression enhanced the effect of carbon ion irradiation in inhibiting the growth of subcutaneous tumors in nude mice. These findings provide the foundation for the development of the STAT1-HO-1 axis as a radiosensitization target for LUAD patients.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4265-4281"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143634297","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":"Human umbilical cord mesenchymal stem cell exosomes promote elastin production and acute skin wound healing via TGFβ1-Smad pathway.","authors":"Yi Zi, Jie Li, XinPing Qian, Jian Li, Yan Jin, ZiBo Zhang, YanHua Jin","doi":"10.1007/s11010-025-05264-5","DOIUrl":"10.1007/s11010-025-05264-5","url":null,"abstract":"<p><p>Skin wound healing is a complex physiological process influenced by multiple factors, including the patient's overall health status. Exosomes derived from human umbilical cord mesenchymal stem cells (hUCMSC-Exos) have demonstrated significant potential in enhancing wound repair. This study investigates the mechanisms through which hUCMSC-Exos facilitate skin wound healing and evaluates their potential application in combination with hydrogels for clinical treatment. Human foreskin fibroblasts (HFF-1) were treated with varying concentrations of hUCMSC-Exos to evaluate their impact on cell proliferation, assessed via the CCK-8 assay. Exosome uptake by HFF-1 cells was visualized using PKH-26 dye staining, while flow cytometry was employed to analyze cell cycle changes. Cell migration was evaluated through scratch and Transwell assays. Gene expression levels of Collagen I, Elastin, and Fibronectin were quantified by qRT-PCR, while Elastin secretion was measured by ELISA. Western blotting was used to examine proteins in the TGFβ1-Smad signaling pathway. The role of SP1 in regulating Elastin gene expression was investigated by testing the SP1 inhibitor Plicamycin and examining hUCMSC-Exos ability to counteract its effect. Additionally, a chromatin immunoprecipitation (ChIP) assay was performed to analyze SP1 binding at the Elastin gene promoter. In vivo, the efficacy of hUCMSC-Exos combined with hydrogels in promoting wound healing was assessed using a mouse skin wound model. hUCMSC-Exos significantly enhanced HFF-1 cell proliferation at concentrations exceeding 1 × 10⁹ particles/mL and increased the proportion of cells in the S and G2/M phases. HFF-1 cells readily absorbed these exosomes, leading to improved cell migration. Treatment with hUCMSC-Exos upregulated the gene expression of Collagen I, Fibronectin, and Elastin. The SP1 inhibitor Plicamycin reduced Elastin gene expression, an effect that was reversed by hUCMSC-Exos. In vivo, the combination of hUCMSC-Exos and hydrogels accelerated wound healing, enhanced collagen organization, and promoted the formation of elastic fibers and blood vessels. hUCMSC-Exos facilitate skin wound healing by promoting SP1 binding to the Elastin gene promoter, thereby upregulating Elastin expression and supporting extracellular matrix remodeling. These findings suggest a promising therapeutic role for hUCMSC-Exos in clinical applications for wound healing.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4499-4511"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811774","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":"Molecular characterization underlying IFN-α2 treatment in polycythemia vera: a transcriptomic overview.","authors":"Fang-Fang Liu, Ke Li","doi":"10.1007/s11010-025-05238-7","DOIUrl":"10.1007/s11010-025-05238-7","url":null,"abstract":"<p><p>Polycythemia vera (PV) is the most common chronic myeloproliferative neoplasm (MPN) in adults. Pegylated interferon-α2 (IFN-α2) is an effective and safe drug for the treatment of PV. However, the mechanisms of its action in PV are still not fully understood. Using the WGCNA and Limma algorithm, we found a subset of IFN-α2 sensitive genes and four gene co-expression modules. Meanwhile, we also found 820 genes were differentially expressed in PV compared with healthy controls. By integrating the above results, several differentially expressed genes (DEGs) that were up- or down-regulated in PV but showed opposite alterations in the IFN-α2-treated group were found. These genes were mainly related to three types of biological processes (metal ion homeostasis, metabolic/catabolic process, and Jak-STAT signaling pathway), the dysfunctions of which were prevalent in PV. Moreover, we applied another threshold-free analysis method to compare global gene expression between IFN-α2 treated PV, PV, and control groups. Results showed the transcriptome changes of PV versus controls were negatively correlated with that of IFN-α2 treated versus untreated PV, indicating IFN-α2 treatment could partially reverse the dysregulated gene expression profile due to PV pathology. In summary, interferon may alleviate the progression of PV through multiple pathways. The findings may be of assistance in understanding the molecular basis underlying this treatment.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4169-4181"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143542634","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":"SKA3 promotes lung adenocarcinoma progression via the EGFR/E2F1/SKA3/integrin β1 signaling loop.","authors":"Xiufen Zheng, Zedong Sun, Shi Wang, Qibing Liu, Biqing Zhu, Zhijian Ren, Dingwei Fan, Chunping Zhang, Xinyin Fu, Yan Jin, Jing Luo, Jie Wang, Binhui Ren","doi":"10.1007/s11010-025-05242-x","DOIUrl":"10.1007/s11010-025-05242-x","url":null,"abstract":"<p><p>Spindle and kinetochore-associated complex subunit 3 (SKA3) contributes to tumor growth and metastasis, but its specific roles have not been clearly elucidated. In this study, we found that SKA3 contributed to lung adenocarcinoma (LUAD) progression by interacting with integrin β1. The expression characteristics of SKA3 in LUAD patients were analyzed by The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets and validated in 33 paired LUAD tissues by immunohistochemistry. Our data confirmed that SKA3 was a crucial regulator of LUAD progression and was associated with worse patient survival. In vitro and in vivo studies showed that SKA3 increased cell migration and invasion. Mechanistically, it was demonstrated that SKA3 could bind to integrin β1 and promote its activation, which further promoted the activation of EGFR. As a positive feedback loop, the activation of EGFR in turn promoted the expression of SKA3 via E2F1-mediated transcriptional regulation. Inhibition of EGFR with AZD9291 blocked SKA3 signaling induced by E2F1. These results indicated that SKA3 was crucial for the activation of EGFR and its downstream signaling pathway. Our findings uncovered the oncogenic role of SKA3 in LUAD progression and elucidated a novel EGFR/E2F1/SKA3/integrin β1 signaling loop, providing a potential SKA3-directed therapeutic strategy for LUAD patients.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4213-4226"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582325","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":"Single-cell RNA sequencing generates an atlas of normal tibia cartilage under mechanical loading conditions.","authors":"Junjie Wang, Zewen Sun, Chenghao Yu, Haibo Zhao, Mingyue Yan, Shenjie Sun, Xu Han, Tianrui Wang, Yingze Zhang, Jianjun Li, Tengbo Yu","doi":"10.1007/s11010-025-05234-x","DOIUrl":"10.1007/s11010-025-05234-x","url":null,"abstract":"<p><p>Chondrocytes in articular cartilage can secrete extracellular matrix to maintain cartilage homeostasis. It is well known that articular cartilage chondrocytes are sensitive to mechanical loading and that mechanical stimuli can be translated to biological processes. This study provides deep insight into the impact of mechanical loading on chondrocytes via single-cell RNA sequencing (scRNA-seq). Five cartilage tissue samples from the high-loading region of medial cartilage from the upper tibia (the TL group) and six cartilage tissue samples from the low-loading region of lateral cartilage from the upper tibia (the TN group) were obtained from six donors and subjected to scRNA-seq. TL and TN cartilage tissues from another donor were subjected to immunohistochemical staining. In total, 132,685 cells were analyzed and assigned to 11 cell types. The functions, developmental relationships and interactions of these cell types were determined, and gene transcription data were also evaluated. In addition, differentially expressed genes between the TL and TN groups and their functions were identified. The hub genes for the TL group were identified as GAPDH, FN1, VEGFA, LDHA, SOD1, CTGF, DCN, SERPINE1, ENO1 and CAV1, whereas the hub genes for the TN group included ACTB, CD44, MMP2, COL1A1, COL1A2, SPP1, CTGF, MYC, CCL2, and IGF1. The different enrichment terms indicated that physiological mechanical loading may induce reactive oxygen species accumulation and thus cause ferroptosis in chondrocytes.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4243-4257"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616009","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":"Association between herpesviruses and alzheimer's disease: a meta-analysis based on case-control studies.","authors":"Huilin Feng, Kexiao Pan, Zulfa Ismail Shabani, Hongju Wang, Wenqiang Wei","doi":"10.1007/s11010-025-05263-6","DOIUrl":"10.1007/s11010-025-05263-6","url":null,"abstract":"<p><p>Herpesviruses infection has been found to be implicated in the etiology of Alzheimer's disease (AD). However, the results remain controversial. This systematic meta-analysis was aimed to evaluate the relationship between Herpesviruses infection and the risk of developing AD. Relevant literature was searched from five databases, including CNKI, PubMed, Web of Science, Embase, and Cochrane Library, to obtain case-control studies (published between the date of database establishment and February 2025; no language restrictions) that compared the Herpesviruses positivity in AD patients and healthy controls. Among all existing studies, there are more abundant published case-control studies on the relationship between HSV-1, HCMV and Alzheimer's disease. Therefore, we chose these two viruses to further explore their association with Alzheimer's disease. The quality of the included studies was evaluated by the NOS scale. The Review Manager 5.3 software was used to calculate the odds ratio (OR) and 95% confidence interval (95% CI) for meta-analysis. Publication bias was investigated using the funnel plots, Begg's and Egger's publication bias plots. Twenty-one eligible studies were included to investigate the association between HSV-1 and AD. The results of the meta-analysis indicated that HSV-1 infection is a risk factor for AD (OR = 1.39, 95% CI = (1.14-1.69), P < 0.05)). In the subgroup analysis, the pooled ORs of HSV-1 infection associated with AD were 1.28 (95% CI: 0.74-2.22) in literature prior to 2010;1.44 (95% CI: 1.14-1.82) in literature after 2010; 1.27(95% CI: 1.01-1.60) in studies from Europe; 1.22(95% CI: 0.66-2.27) in studies from North America;1.89 (95% CI: 1.19-3.02) in studies from Asia; 1.38 (95% CI: 1.10-1.74) in the clinical diagnosis group; 1.52 (95% CI: 0.84-2.74) in the autopsy group. The pooled OR of APOE4 positivity and AD risk was 5.51 (95% CI: 4.33-7.01). The association between HCMV and AD was analyzed in seven studies. The pooled result showed that HCMV infection is not a risk factor for AD (OR = 0.83, 95% CI = 0.63-1.09). Our latest meta-analysis suggests that HSV-1 infection is a risk factor for the risk of AD. Therefore, anti-HSV-1 infection can serve as a potential therapeutic strategy for control of AD incidence. There is insufficient evidence to support association between HCMV and AD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4079-4090"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720554","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":"Sodium butyrate attenuates liver fibrogenesis via promoting H4K8 crotonylation.","authors":"Ruiqi Tang, Hua Zha, Rongrong Liu, Jiawen Lv, Dan Cao, Lanjuan Li","doi":"10.1007/s11010-025-05274-3","DOIUrl":"10.1007/s11010-025-05274-3","url":null,"abstract":"<p><p>Sodium butyrate (NaB), a histone deacetylase (HDAC) inhibitor derived from dietary sources, demonstrates its potential in improving liver fibrosis in mice. This study explored NaB's impact on liver fibrosis through histone crotonylation. In vitro, NaB significantly inhibited the growth of TGF-β-stimulated LX2 hepatic stellate cells and reduced the expression of fibrotic markers ACTA2, the encoding gene of αSMA, and COL1A1 proportionally to the dosage. In vivo, NaB treatment of CCl₄-induced ICR mice led to notable gains in liver function and a marked suppression in liver fibrosis. NaB inhibited Hdac2 and Hdac3 expression leading to increased H4K8 crotonylation, and modulated key fibrosis-related genes, providing a mechanistic basis for its therapeutic potential. Trichostatin A (TSA) exhibited similar effects to NaB, supporting the importance of HDAC inhibition in modulating these pathways. Overall, NaB's modulation of HDAC activity and histone crotonylation reveals a novel mechanism underlying its impact on liver fibrosis, highlighting its promise as a treatment for liver disease.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4467-4481"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779714","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":"Chloride channels and mast cell function: pioneering new frontiers in IBD therapy.","authors":"Ahmed M Aljameeli, Bader Alsuwayt, Deepak Bharati, Vaishnavi Gohri, Popat Mohite, Sudarshan Singh, Vijay Chidrawar","doi":"10.1007/s11010-025-05243-w","DOIUrl":"10.1007/s11010-025-05243-w","url":null,"abstract":"<p><p>Emerging evidence indicates that chloride channels (ClCs) significantly affect the pathogenesis of inflammatory bowel disease (IBD) through their regulatory roles in mast cell function and epithelial integrity. IBD, encompassing conditions such as Crohn's disease and ulcerative colitis, involves chronic inflammation of the gastrointestinal tract, where channels influence immune responses, fluid balance, and cellular signalling pathways essential for maintaining mucosal homeostasis. This review examines the specific roles of ClC in mast cells, focussing on the regulation of mast cell activation, degranulation, cytokine release, and immune cell recruitment in inflamed tissues. Key channels, including Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) and ClC-2, are discussed in detail because of their involvement in maintaining intestinal epithelial barrier function, a critical factor disrupted in IBD. For example, CFTR facilitates chloride ion transport across epithelial cells, which is essential for mucosal hydration and maintenance of the intestinal barrier. Reduced CFTR function can compromise this barrier, permitting microbial antigens to penetrate the underlying tissues and triggering excessive immune responses. ClC-2, another chloride channel expressed in mast cells and epithelial cells, supports tight junction integrity, contributes to barrier function, and reduces intestinal permeability. Dysregulation of these channels is linked to altered mast cell activity and excessive release of pro-inflammatory mediators, exacerbating IBD symptoms, such as diarrhoea, abdominal pain, and tissue damage. Here, we review recent pharmacological strategies targeting ClC, including CFTR potentiators and ClC-2 activators, which show the potential to mitigate inflammatory responses. Additionally, experimental approaches for selective modulation of chloride channels in mast cells have been explored. Although targeting ClC offers promising therapeutic avenues, challenges remain in achieving specificity and minimizing side effects. This review highlights the therapeutic potential of Cl channel modulation in mast cells as a novel approach for IBD treatment, aiming to reduce inflammation and restore intestinal homeostasis in affected patients.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3951-3969"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557354","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":"Adiponectin mediated metabolic and sphingolipid alterations in preventing endothelial dysfunction.","authors":"Vinnyfred Vincent, Himani Thakkar, Atanu Sen, Ashutosh Bansal, Ujjalkumar Subhash Das, Abishek Gunasekaran, Neerja Bhatla, Thirumurthy Velpandian, Archna Singh","doi":"10.1007/s11010-025-05268-1","DOIUrl":"10.1007/s11010-025-05268-1","url":null,"abstract":"<p><p>Endothelial dysfunction is an early indicator of atherosclerosis. Adiponectin, a hormone secreted by adipose tissue with insulin-sensitizing and anti-inflammatory properties, offers protection against atherosclerosis. This study investigated the metabolic and sphingolipid alterations in endothelial cells linked to the protective effects of adiponectin against endothelial dysfunction. Human Umbilical Endothelial Cells (HUVECs) were treated with Tumor Necrosis Factor-alpha (TNF-α) to induce endothelial dysfunction. AdipoRon and SKI-I were used to study the effects of adiponectin and sphingosine kinase inhibition in HUVECs. Metabolic changes and sphingolipid alterations were assessed to understand changes in lipid metabolism, and RNA sequencing was used to quantify the transcriptomics changes. TNF-α treatment significantly upregulated glycolysis and downregulated long-chain fatty acid oxidation and mitochondrial ATP production, while AdipoRon co-treatment partially reversed these metabolic effects. In HUVECs, TNF-α treatment increased intracellular C16 and C18 ceramides and Sphingosine 1-Phosphate (S1P) while decreasing extracellular S1P. AdipoRon Co-treatment reversed these effects; AdipoRon also reversed the transcriptional changes induced by TNF-α. Sphingosine kinase inhibition in HUVECs led to mitochondrial dysfunction at the metabolic and transcriptional levels. This study provides insights into potential therapeutic strategies targeting endothelial metabolism while unraveling a novel mitochondrial modulation mediated by sphingosine kinases in endothelial cells.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4365-4377"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720553","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":"PUS7 promotes the progression of pancreatic cancer by interacting ANLN to activate MYC pathway.","authors":"Yubo Jiang, Qian Cheng, Yingying Zhang, Jingtao Zhong","doi":"10.1007/s11010-025-05267-2","DOIUrl":"10.1007/s11010-025-05267-2","url":null,"abstract":"<p><p>To investigate the role of pseudouridine synthase 7 (PUS7) in pancreatic cancer (PC) and explore its underlying molecular mechanisms. PUS7 role in the malignant biological function of PC cells was investigated by colony formation, EdU, flow cytometry, and transwell assays. PUS7 function on glycolysis of PC cells was determined through assessing the extracellular acidification rate and oxygen consumption rate. Besides, the potential molecular mechanism by which PUS7 affects PC was investigated via utilizing immunohistochemistry staining, western blot, qRT-PCR, and co-immunoprecipitation. Xenograft tumors were constructed using BALB/c nude mice. PUS7 was highly expressed in PC tissues. PUS7 significantly accelerated proliferation, mobility and glycolysis, but suppressed apoptosis in PC. Furthermore, PUS7 promoted the malignant biological function of PC cells by interacting anillin (ANLN). We also demonstrated that PUS7 promoted the malignant biological function of PC cells by activating the MYC pathway. PUS7 promoted PC progression via activating the MYC pathway in vivo. Our results indicated that PUS7 could promote cell proliferation, mobility and glycolysis, and inhibit apoptosis by interacting ANLN to activate the MYC pathway in PC.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4401-4415"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764372","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}