Critical Reviews in Eukaryotic Gene Expression最新文献

{"title":"Glycyrrhizin Alleviates Puromycin Aminonucleoside-Induced Podocyte Injury via Regulating Autophagy and GSDMD-Dependent Pyroptosis.","authors":"Wei Lu, Sheng-You Yu, Li-Na Wang, Yao-Zhang, Qiao-Qun Ou, Yuan-Chun Liu, Li Yu","doi":"10.1615/CritRevEukaryotGeneExpr.2025058852","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025058852","url":null,"abstract":"<p><p>Podocyte damage contributes to the progression of various renal diseases. This study aimed to investigate the effects of glycyrrhizin (GL) on podocyte injury. Puromycin aminonucleoside (PAN) was used to establish podocyte injury model in vitro. High throughput sequencing was applied for analyzing the differentially expressed genes (DEGs). Kyoto Encyclopedia of Genes and Genomes was used to analyze the enrichment of DEGs. Gene expression was detected using Western blot and reverse transcription-quantitative PCR. The cytokine release was detected using enzyme-linked immunosorbent assay. Cytotoxicity was detected using lactate dehydrogenase assay. The death of podocytes was detected using terminal deoxynucleotidyl transferase dUTP nick-end labeling assay and flow cytometry. We found that the DEGs after exposure to PAN were enriched in inflammatory signaling and autophagy. However, GL treatment suppressed the release of proinflammatory cytokines. GL treatment abrogated the effects of PAN and upregulated phosphorylated unc-51 like autophagy activating kinase 1, Beclin1, autophagy related 5, LC3B/A, lysosomal associated membrane protein 2, whereas downregulated sequestosome 1 and gasdermin D. Moreover, GL treatment suppressed the cytotoxicity induced by PAN as well as the pyroptosis of podocytes. However, 3-Methyladenine-mediated autophagy inhibition promoted the inflammation and pyroptosis of podocytes. In summary, GL exerts protective effects on PAN-induced podocyte injury. GL-mediated activation of autophagy suppresses inflammation and pyroptosis of podocytes. Therefore, GL may be a therapeutic strategy for podocyte injury.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 5","pages":"69-80"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144327892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the Transcription Factor FoxO in Type 2 Diabetes and Its Complications.","authors":"Jing Hui Shi, Yi Biao Shi, Si Tian Qiu, Ying Song","doi":"10.1615/CritRevEukaryotGeneExpr.2025057309","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2025057309","url":null,"abstract":"<p><p>FoxO proteins represent a subfamily of the forkhead box family (Fox) superfamily of proteins. It is involved in cell proliferation, differentiation, oxidative stress, apoptosis as well as tumors and metabolic disorders by regulating cellular functions. This paper aims to summarize the role of the transcription factor FoxO in type 2 diabetes and its complications, which may add to the potential of FoxO as a therapeutic target for future research. The transcription factor FoxO is expressed in various tissues and participates in various bodily functions including cell proliferation, differentiation, apoptosis, tumor therapy, and metabolic processes, playing a crucial role in the human body. FoxO plays a positive role in attenuating oxidative stress, inflammation, and metabolic disorders, which are the main causes of type 2 diabetes and its complications. FoxO plays an important role in the regulation of type 2 diabetes and its complications, and more precise targeting studies of FoxO will help to prevent, regulate, and treat diabetes-related diseases.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 3","pages":"85-103"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Ferroptosis-Associated Genes in Primary Open-Angle Glaucoma through Bioinformatics Analysis.","authors":"Dongmei Hong","doi":"10.1615/CritRevEukaryotGeneExpr.2025057767","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025057767","url":null,"abstract":"<p><p>This study aims to examine ferroptosis-associated genes in primary open-angle glaucoma (POAG) and offer new insights into the underlying disease mechanisms and potential therapeutic approaches. Differentially expressed genes (DEGs) between the POAG and control groups were identified using bioinformatics analysis and subsequently intersected with a ferroptosis gene set to isolate ferroptosis-related DEGs (Ferr DEGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to examine their biological functions. Core genes were identified through protein-protein interaction (PPI) network and Friends analysis. The diagnostic potential of core Ferr DEGs was assessed using receiver operating characteristic (ROC) curve analysis, while immune cell infiltration was examined using the CIBERSORT algorithm. Additionally, Spearman correlation analysis was used to examine the relationships between the identified genes and immune cell populations. A total of 25 Ferr DEGs were identified, with DDIT4, GDF15, NAMPT, HBA1, and IGFBP7 recognized as key core genes. ROC analysis demonstrated that these genes exhibited high diagnostic accuracy, with an AUC > 0.7. Additionally, the infiltration levels of memory B cells and macrophage_M2 were significantly elevated in POAG tissues compared to the control group. Notably, the core genes revealed significant correlations with various immune cell types. Our findings underscore the involvement of ferroptosis-related genes in POAG pathogenesis and highlight their potential as diagnostic biomarkers and therapeutic targets. Future research should focus on validating these findings in clinical settings and exploring the therapeutic modulation of ferroptosis in POAG management.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 4","pages":"15-26"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144024248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic Values of Homocysteine and Potassium Levels in Acute Ischemic Stroke Patients after Intravenous Thrombolysis with Recombinant Tissue-Type Plasminogen Activator.","authors":"Keliang Li, Min Xu, Yun Zhang, Lipeng Zhao","doi":"10.1615/CritRevEukaryotGeneExpr.2024055719","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024055719","url":null,"abstract":"<p><p>Abnormal levels of homocysteine (Hcy) and potassium are associated with poor prognosis of patients with ischemic stroke. Nonetheless, the roles Hcy and potassium in the prognosis of patients with acute ischemic stroke (AIS) receiving intravenous thrombolysis (IVT) with recombinant tissue-type plasminogen activator (rt-PA) are still unknown. Therefore, the purpose of this study is to investigate the association between the levels of Hcy and potassium and clinical prognosis in AIS patients receiving IVT with rt-PA. AIS patients receiving IVT with rt-PA were enrolled in this study. AIS patients were divided into early neurological deterioration (END) and no END group according to the National Institutes of Health Stroke Scale (NIHSS) scores. Moreover, patients were divided into favorable outcome and poor outcome according to the modified Rankin Scale (mRS) scores. Multivariate logistic regression analysis was applied for detecting the risk factors. Four-hundred-twenty-six patients with AIS IVT with rt-PA were recruited: 24 patients showed END within 24 h. One-hundred-fifty-seven patients showed poor outcome. Multivariate analysis showed that higher levels of Hcy level (P < 0.001) and lower levels of potassium level (P < 0.01) were more frequently in patients with END and poor outcomes in AIS patients with IVT at the three-month visit. Taken together, the high Hcy and low potassium levels may be the potential biomarker for AIS patients receiving IVT with rt-PA.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"65-73"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIP13 Is a Potential Prognostic Marker and Therapeutic Target for Endometrial Cancer.","authors":"Zengzhen Lai, Chaolin Li","doi":"10.1615/CritRevEukaryotGeneExpr.2025056929","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2025056929","url":null,"abstract":"<p><p>Uterine corpus endometrial carcinoma (UCEC) is a prevalent malignancy within the female reproductive system, with a rising global incidence. Although thyroid hormone receptor interacting protein 13 (TRIP13) has been implicated in various tumor etiologies and progressions, its role in UCEC remains poorly characterized. This study aimed to delineate TRIP13's expression profile in UCEC by analyzing transcriptome data from multiple databases. We investigated genomic alterations and epigenetic modifications of the TRIP13 gene using the cBioPortal tool. The prognostic value of TRIP13 was assessed via Kaplan-Meier survival analysis and Cox regression modeling. Additionally, we examined TRIP13's impact on immunotherapy responsiveness and chemotherapy sensitivity through immunological and pharmacological analyses. The expression of TRIP13 in both normal endometrial and cancer cell lines was evaluated using quantitative real-time polymerase chain reaction (qPCR). Our findings reveal that TRIP13 expression in UCEC tumor samples is significantly higher than in normal tissues and increases with tumor grade and stage progression. High TRIP13 expression is significantly associated with poor prognosis in UCEC patients, establishing it as an independent prognostic biomarker. TRIP13 shows a positive correlation with immunosuppressive cell infiltration and a negative correlation with immune-activating cell infiltration, suggesting a potential role in tumor immune evasion. Further analysis identified TRIP13 as a potential biomarker for predicting immunotherapy response. Moreover, TRIP13 expression is significantly associated with sensitivity to certain chemotherapeutic agents, indicating its potential as a therapeutic target. qPCR experiments confirmed the overexpression of TRIP13 in endometrial cancer cell lines. The role of TRIP13 in modulating the tumor immune microenvironment, as well as its predictive value for immunotherapy and chemotherapy responses, underscores its importance in developing personalized treatment strategies for UCEC. These findings provide novel molecular targets and therapeutic insights for a precision medicine approach to UCEC.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 3","pages":"23-41"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of Curcumin Inhibition of Malignant Progression of Lung Cancer Cells by Regulating Ferroptosis via the NRF2/HMOX1 Pathway.","authors":"Xiaoqi Guo, Tianci Han, Liang Zhang","doi":"10.1615/CritRevEukaryotGeneExpr.2025058526","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025058526","url":null,"abstract":"<p><p>Inducing ferroptosis has become a means of hindering lung cancer progression. Curcumin regulates ferroptosis and participates in lung cancer progression, yet its mechanism on ferroptosis remains unclear. Semaphorin-6A attenuates lung cancer cell migration through the nuclear factor erythroid-2-related factor 2 (NRF2)/heme oxygenase-1 gene (HMOX1) axis. Therefore, the study investigated the mechanism of curcumin inhibiting the malignant progression of lung cancer cells by regulating ferroptosis via the NRF2/HMOX1 pathway. A549 and H209 cell viability, proliferation, death, invasion and migration were assessed by CCK-8, colony formation, lactate dehydrogenase, and Transwell assays. Levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and Fe2+, glutathione peroxidase 4 (GPX4), nuclear NRF2, and HMOX1, and NRF2 nuclear translocation were measured by kits, Western blot and immunofluorescence. Cell viability, proliferation, invasion and migration were decreased after curcumin treatment, while cell death was significantly increased (all P < 0.01). Curcumin-treated cells showed elevated ROS, MDA and Fe2+ levels, decreased SOD, GSH and GPX4 levels (all P < 0.01), and increased nuclear NRF2 level and nuclear translocation, and HMOX1 expression (all P < 0.01), suggesting that curcumin activated the NRF2/HMOX1 pathway to promote ferroptosis, thereby inhibiting lung cancer cell malignant progression. Liproxstatin-1 or ML385 treatment reversed curcumin-induced anti-tumor effect and ferroptosis. Curcumin activates the NRF2/HMOX1 pathway to promote ferroptosis, thus repressing the malignant progression of lung cancer cells. These findings provide new insights into the mechanism of curcumin's anti-tumor effect and highlight its potential as a therapeutic drug for lung cancer.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 5","pages":"39-51"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144327808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL14 Inhibits the Pyroptosis of Neurons in Parkinson's Disease via Upregulating NFE2.","authors":"Xiaoli Hou, Ming Li, Huishen Yan, Hong Cheng","doi":"10.1615/CritRevEukaryotGeneExpr.2025059356","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025059356","url":null,"abstract":"<p><p>Methyltransferase-like 14 (METTL14) has been identified as a protective factor in central nervous system disorders, yet its involvement in Parkinson's disease (PD) remains underexplored. This study aimed to investigate the role of METTL14 in PD. An in vitro PD model was established by exposing neurons to 1-methyl-4-phenylpyridinium (MPP+). mRNA levels were quantified via real-time-quantitative PCR. Protein expression was assessed through Western blot. The release of pyroptosis-related cytokines was detected using enzyme-linked immunosorbent assay. N6-methyladenosine (m6A) levels were measured using an m6A assay. m6A enrichment was pinpointed with a methylated RNA immunoprecipitation assay. The transcriptional activity of nuclear factor, erythroid 2 (NFE2) was evaluated using a luciferase assay. Cell viability, neuronal cytotoxicity, and neuronal death were respectively determined using Cell Counting Kit-8, lactate dehydrogenase, and terminal deoxynucleotidyl transferase dUTP nick-end labeling assays. Our findings unveiled that METTL14 expression is diminished following MPP+ exposure, which in turn triggers neuroinflammation and pyroptosis. Conversely, overexpression of METTL14 mitigates neuroinflammation and pyroptosis, and restores neuronal function. Mechanistically, METTL14 augments the m6A modification of NFE2 at a specific site, thereby preserving its mRNA stability. However, NFE2 knockdown exacerbates neuroinflammation and pyroptosis. In summary, METTL14 safeguards against neurodegeneration in PD by modulating the m6A modification of NFE2, positioning the METTL14/NFE2 axis as a potential therapeutic target for PD.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 6","pages":"47-57"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145093194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kaempferol Inhibits Myocardial Fibrosis by Downregulating FVII.","authors":"Ming Zhang, Zhengbo Zhu, Qian Zhou, Liyun Liu","doi":"10.1615/CritRevEukaryotGeneExpr.v35.i6.10","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.v35.i6.10","url":null,"abstract":"<p><p>Myocardial fibrosis is a critical pathological process in the progression of heart failure and other cardiovascular diseases. Kaempferol (KMP), a natural flavonoid, has antioxidant and anti-inflammatory properties. This study investigates the effects of KMP on myocardial fibrosis. Isoproterenol injection was used to establish myocardial fibrosis mouse model. Cardiac function was assessed by echocardiography. Histology analysis was conducted using Masson assay and Sirius red staining. The expression of survival of motor neuron 1 (α-SMA) and Collagen III was detected using immunohistochemistry. RNA expression was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cytokine release was detected using enzyme-linked immunosorbent assay. Protein expression was detected using Western blot. We found that KMP treatment improved cardiac function as well as suppressed myocardial fibrosis. Moreover, KMP treatment decreased expression of fibrosis-related genes and attenuated inflammation in fibrotic hearts. Furthermore, KMP treatment inhibited the expression of coagulation factor VII (FVII), the overexpression of which promoted inflammation response and myocardial fibrosis. In summary, KMP exerts protective effects against myocardial fibrosis via downregulating FVII. These findings suggest that KMP may be a promising therapeutic candidate for myocardial fibrosis.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 6","pages":"1-10"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145093238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changes in the Levels of the Serum Markers Serum Amyloid A and Immunoglobulin M in Children with Mycoplasma pneumoniae Infection Complicated with Asthma and Their Clinical Significance.","authors":"Shanshan Xiao, Xuejing Hou","doi":"10.1615/CritRevEukaryotGeneExpr.2025056739","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025056739","url":null,"abstract":"<p><p>Asthma represents a chronic disorder with aberrant immunological and inflammatory responses. We analyzed the levels and clinical significance of serum markers serum amyloid A (SAA) and immunoglobulin M (IgM) in Mycoplasma pneumoniae (MP)-infected children with asthma. MP-infected children were allocated into the Asthma (n = 64) and N-Asthma (n = 104) groups, with baseline information collected. Levels of IgE, c-reactive protein, procalcitonin, lactate dehydrogenase, aspartate aminotransferase, interleukin-4/interferon-γ (IL-4/IFN-γ), transforming growth factor β1 (TGF-β1), SAA and IgM were determined by ELISA. Tidal breathing lung function [inspiratory time (TI), expiratory time (TE), inspiratory volume (V-TI), expiratory volume (V-TE), tidal volume (VT) and respiratory rate (RR)] was assessed using a pulmonary function instrument. The relationship of serum SAA and IgM with IgE, IL-4/IFN-γ, TGF-β1, and tidal breathing lung function in MP-infected asthmatic children, and their diagnostic value for asthma occurrence in MP-infected children were analyzed by Spearman analysis and receiver operating characteristic curve. IgE, V-TI, V-TE, VT, IL-4/IFN-γ, TGF-β1, SAA and IgM indexes in MP-infected asthmatic children surpassed those without asthma. Serum SAA and IgM significantly positively correlated with IgE, IL-4/IFN-γ, TGF-β1, V-TI, V-TE and VT, which had certain diagnostic value for asthma in MP-infected children. The incidence of asthma was higher in MP-infected children with high SAA and IgM expression levels. The diagnostic efficacy of SAA and IgM combined test surpassed single detection. Serum SAA and IgM were highly expressed in MP-infected asthmatic children, and their combined detection had high diagnostic value for asthma in MP-infected children.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 4","pages":"27-37"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144051513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NEK6 Accelerates Hepatocellular Carcinoma Progression and Glycolysis through Ubiquitination of TCP10L.","authors":"Ling Su, Dehong Zhao, Cheng Zhou, Biao Zhang","doi":"10.1615/CritRevEukaryotGeneExpr.2025057446","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025057446","url":null,"abstract":"<p><p>Never in mitosis a related kinases 6 (NEK6) is a serine/threonine kinase, and dysregulation of NEK6 is associated with malignant progression of human cancers. Nonetheless, the biological function and molecular mechanism of NEK6 in hepatocellular carcinoma (HCC) are unknown. Our study found that NEK6 was obviously raised in HCC patient tissues and cells, and patients with high NEK6 expression had a worse prognosis. Silencing of NEK6 reduced the growth, metastasis, cell cycle, and glycolysis of HCC cells while facilitating apoptosis. In vivo experiments also showed that NEK6 knockdown dramatically hampered tumor growth, suggesting that NEK6 enhanced HCC progression in vivo and in vitro. Next, we proved that TCP10L was a target gene of NEK6, and NEK6 negatively regulated TCP10L expression. Mechanistically, we confirmed that NEK6 was bound to TCP10L, and NEK6 degraded TCP10L protein expression through ubiquitination. Rescue experiments also declared that TCP10L reversed the effect of NEK6 on HCC cells. Our results disclosed that NEK6 heightened HCC progression and glycolysis through ubiquitination of TCP10L. Our study may provide a new perspective for the treatment of HCC.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 4","pages":"1-13"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}