Journal of cellular biochemistry最新文献

{"title":"Supervillin-Mediated ZO-1 Downregulation Facilitates Migration of Cisplatin-Resistant HCT116 Colorectal Cancer Cells.","authors":"Yali Hong, Xu Li, Rongchen Mao, Feier Zhou, Shengnan Li, Chao Zhu, Lai Jin","doi":"10.1002/jcb.30699","DOIUrl":"https://doi.org/10.1002/jcb.30699","url":null,"abstract":"<p><p>Supervillin (SVIL), the biggest member of the villin/gelsolin superfamily, has recently been reported to promote the metastasis of hepatocellular carcinoma by stimulating epithelial-mesenchymal transition (EMT). However, little is known about the roles of SVIL in the migration of colorectal cancer cells. Here, we investigated the effects of SVIL on the migration of cisplatin-resistant colorectal cancer cells. The model of cisplatin-resistant HCT116 cells (HCT116/DDP) was established. Migration was assessed after SVIL knockdown. Tumor metastasis was assessed using a mouse model with tail vein injection of colorectal cancer cells. The results showed that the expression of SVIL was upregulated in HCT116/DDP cells compared to that in their parental cells. Also, the HCT116/DDP cells showed increased cell migration and lung metastasis. Furthermore, we revealed that the expression of SVIL was associated with the migration of HCT116/DDP cells. Reduced SVIL expression inhibited migration and lung metastasis in HCT116/DDP cells. Further work showed that SVIL knockdown blocked cell migration by targeting zona occludens-1 (ZO-1) mediated tight-junction remodeling. The expression of ZO-1, but not occludin and cludin5, was downregulated after SVIL knockdown. Immunofluorescence indicated that the linear ZO-1 was interrupted while the SVIL knockdown reversed the interruption. This study displayed the relationship between SVIL and ZO-1 in cisplatin-resistant colon cancer cells, providing a new insight into the mechanism of colorectal cancer migration.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":"e30699"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142914932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Sodium-Dependent Vitamin C Transporter-2 and Ascorbate in Regulating the Hypoxic Pathway in Cultured Glioblastoma Cells.","authors":"Eleanor R Burgess, Citra Praditi, Elisabeth Phillips, Margreet C M Vissers, Bridget A Robinson, Gabi U Dachs, George A R Wiggins","doi":"10.1002/jcb.30658","DOIUrl":"10.1002/jcb.30658","url":null,"abstract":"<p><p>The most common and aggressive brain cancer, glioblastoma, is characterized by hypoxia and poor survival. The pro-tumour transcription factor, hypoxia-inducible factor (HIF), is regulated via HIF-hydroxylases that require ascorbate as cofactor. Decreased HIF-hydroxylase activity triggers the hypoxic pathway driving cancer progression. Tissue ascorbate accumulates via the sodium-dependent vitamin C transporter-2 (SVCT2). We hypothesize that glioblastoma cells rely on SVCT2 for ascorbate accumulation, and that knockout of this transporter would disrupt the regulation of the hypoxic pathway by ascorbate. Ascorbate uptake was measured in glioblastoma cell lines (U87MG, U251MG, T98G) by high-performance liquid chromatography. CRISPR/Cas9 was used to knockout SVCT2. Cells were treated with cobalt chloride, desferrioxamine or 5% oxygen, with/without ascorbate, and key hypoxic pathway proteins were measured using Western blot analysis. Ascorbate uptake was cell line dependent, ranging from 1.7 to 11.0 nmol/10⁶ cells. SVCT2-knockout cells accumulated 90%-95% less intracellular ascorbate than parental cells. The hypoxic pathway was induced by all three stimuli, and ascorbate reduced this induction. In the SVCT2-knockout cells, ascorbate had limited effect on the hypoxic pathway. This study verifies that intracellular ascorbate is required to suppress the hypoxic pathway. As patient survival is related to an activated hypoxic pathway, increasing intra-tumoral ascorbate may be of clinical interest.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":" ","pages":"e30658"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Long Non-Coding RNA LOC554202 Promotes Laryngeal Squamous Cell Carcinoma Progression Through Regulating MiR-31.","authors":"","doi":"10.1002/jcb.30695","DOIUrl":"https://doi.org/10.1002/jcb.30695","url":null,"abstract":"<p><strong>Retraction: </strong>S. Yang, J. Wang, W. Ge, and Y. Jiang, \"Long Non-Coding RNA LOC554202 Promotes Laryngeal Squamous Cell Carcinoma Progression Through Regulating MiR-31,\" Journal of Cellular Biochemistry 119, no. 8 (2018): 6953-6960, https://doi.org/10.1002/jcb.26902. The above article, published online on 8 May 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl, and Wiley Periodicals LLC. The expression of concern has been agreed due to third-party concerns related to the data presented in the article. Indicators for cloned image elements and inappropriate undeclared image modification were found in Figure 3D. Furthermore, several statements in the introduction are not sufficiently supported by the cited literature. Finally, the statements in the text referring to Figures 1C and 2C contradict the conclusions supported by the data. Accordingly, the article is retracted as the editors have lost confidence in the data presented.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":"e30695"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 Insight Into YefM-YoeB Complex of Toxin-Antitoxin System From Streptococcus pneumoniae.","authors":"Do-Hee Kim, Yong-Chan Lee, Chenglong Jin, Sung-Min Kang, Su-Jin Kang, Hoon-Seok Kang, Bong-Jin Lee","doi":"10.1002/jcb.30672","DOIUrl":"10.1002/jcb.30672","url":null,"abstract":"<p><p>Streptococcus pneumonia is a Gram-positive and facultative anaerobic bacterium that causes a number of diseases, including otitis media, community-acquired pneumonia, sepsis, and meningitis. With the emergence of antibiotic-resistant strains, there is an urgent need to develop antibiotics with a novel mechanism. The toxin-antitoxin (TA) system, which is primarily found in prokaryotes, consists of a toxin and its equivalent antitoxin genes. The YefM-YoeB module is a Type II TA system, where the YoeB toxin functions as a putative mRNA interferase upon activation, while the YefM antitoxin acts as a transcription repressor by binding to its promoter region along with YoeB. In this study, we determined the crystal structure of the YefM-YoeB complex from S. pneumoniae TIGR4 to comprehend the binding mechanism of the TA system. Furthermore, an in vitro ribonuclease activity assay was conducted to identify the ribonuclease activity of the YoeB toxin. Additionally, furthermore, the oligomeric state of the YefM-YoeB complex in solution was investigated, and a DNA-binding mode was proposed. These structural and functional insights into the YefM-YoeB complex could provide valuable information for the development of novel antibiotics targeting S. pneumonia-associated diseases.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":" ","pages":"e30672"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Notification to \"Procaine Is a Specific DNA Methylation Inhibitor With Anti-Tumor Effect for Human Gastric Cancer\".","authors":"","doi":"10.1002/jcb.30700","DOIUrl":"https://doi.org/10.1002/jcb.30700","url":null,"abstract":"","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":"e30700"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Silico Hybridization and Molecular Dynamics Simulations for the Identification of Candidate Human MicroRNAs for Inhibition of Virulent Proteins' Expression in Staphylococcus aureus.","authors":"Harshita Tiwari, Subhadip Saha, Monidipa Ghosh","doi":"10.1002/jcb.30684","DOIUrl":"10.1002/jcb.30684","url":null,"abstract":"<p><p>Staphylococcus aureus is a major threat to human health, causing infections that range in severity from moderate to fatal. The rising rates of antibiotic resistance highlight the critical need for new therapeutic techniques to combat this infection. It has been recently discovered that microRNAs (miRNAs) are essential for cross-kingdom communication, especially when it comes to host-pathogen interactions. It has been demonstrated that these short noncoding RNAs control gene expression in the gut microbiota, maintaining homeostasis; dysbiosis in this system has been linked to several diseases, including cancer. Our research attempts to use this understanding to target specific bacterial species and prevent severe diseases. In particular, we look for putative human miRNAs that can attach to virulent bacterial proteins' mRNA and prevent them from being expressed. In-silico hybridization experiments were performed between 100 human miRNA sequences with varied expression levels in gram-positive bacterial infections and five virulence factor genes. In addition, these miRNAs' binding properties were investigated using molecular dynamics (MD) simulations. Our findings demonstrate that human miRNAs can target and inhibit the expression of bacterial virulent genes, thereby opening up new paths for developing innovative miRNA-based therapeutics. The implementation of MD simulations in our study not only improves the validity of our findings but also proposes a new method for constructing miRNA-based therapies against life-threatening bacterial infections.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":" ","pages":"e30684"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11735889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lnc-Pim1 Promotes Neurite Outgrowth and Regeneration of Neuron-Like Cells Following ACR-Induced Neuronal Injury.","authors":"He Li, Ruo Yu Jiang, Ya Jie Tang, Cong Ling, Fang Liu, Jia Jun Xu","doi":"10.1002/jcb.30659","DOIUrl":"10.1002/jcb.30659","url":null,"abstract":"<p><p>Decreased regenerative capacity of central nervous system neurons is the main cause for failure of damaged neuron regeneration and functional recovery. Long noncoding RNAs (lncRNAs) are abundant in mammalian transcriptomes, and many time- and tissue-specific lncRNAs are thought to be closely related to specific biological functions. The promoting effect of Pim-1 gene on neural differentiation and regeneration has been documented, but the effect and mechanism of its neighbor gene Lnc-Pim1 in regulating the response of central neurons to injury remain unclear. RT-PCR in this study demonstrated that the expression of Lnc-Pim1 was upregulated in acrylamide (ACR)-induced neuronal injury. FISH and nucleus-cytoplasmic assay demonstrated that Lnc-Pim1 was mainly expressed in the neuron cytoplasm, with a small amount in the nucleus. Western blot analysis proved that Lnc-Pim1 overexpression induced by the lentivirus vector could promote neurite outgrowth in Neuro-2a cells by activating the Erk1/2 signal pathway, and improve neurite regeneration of injured neurons by upregulating GAP-43 and β-Ⅲ tubulin protein expression. However, silencing Lnc-Pim1 expression by interfering RNA could effectively downregulate the GAP-43 and β-Ⅲ tubulin protein expression, and inhibit neurite growth of neurons. In addition, CHIRP-MS was performed to identify several potential targets of Lnc-Pim1 involved in the regulation of neurite regeneration of injured neurons. In conclusion, our study demonstrated that Lnc-Pim1 is a potential lnc-RNA, playing an important role in regulating central nerve regeneration.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":" ","pages":"e30659"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PLM-T3SE: Accurate Prediction of Type III Secretion Effectors Using Protein Language Model Embeddings.","authors":"Mengru Gao, Chen Song, Taigang Liu","doi":"10.1002/jcb.30642","DOIUrl":"10.1002/jcb.30642","url":null,"abstract":"<p><p>The Type III secretion effectors (T3SEs) are bacterial proteins synthesized by Gram-negative pathogens and delivered into host cells via the Type III secretion system (T3SS). These effectors usually play a pivotal role in the interactions between bacteria and hosts. Hence, the precise identification of T3SEs aids researchers in exploring the pathogenic mechanisms of bacterial infections. Since the diversity and complexity of T3SE sequences often make traditional experimental methods time-consuming, it is imperative to explore more efficient and convenient computational approaches for T3SE prediction. Inspired by the promising potential exhibited by pre-trained language models in protein recognition tasks, we proposed a method called PLM-T3SE that utilizes protein language models (PLMs) for effective recognition of T3SEs. First, we utilized PLM embeddings and evolutionary features from the position-specific scoring matrix (PSSM) profiles to transform protein sequences into fixed-length vectors for model training. Second, we employed the extreme gradient boosting (XGBoost) algorithm to rank these features based on their importance. Finally, a MLP neural network model was used to predict T3SEs based on the selected optimal feature set. Experimental results from the cross-validation and independent test demonstrated that our model exhibited superior performance compared to the existing models. Specifically, our model achieved an accuracy of 98.1%, which is 1.8%-42.4% higher than the state-of-the-art predictors based on the same independent data set test. These findings highlight the superiority of the PLM-T3SE and the remarkable characterization ability of PLM embeddings for T3SE prediction.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":" ","pages":"e30642"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Revisiting Luteolin Against the Mediators of Human Metastatic Colorectal Carcinoma: A Biomolecular Approach.","authors":"Ankita Chakraborty, Advaitha Midde, Pritha Chakraborty, Sourin Adhikary, Simran Kumar, Navpreet Arri, Nabarun Chandra Das, Parth Sarthi Sen Gupta, Aditi Banerjee, Suprabhat Mukherjee","doi":"10.1002/jcb.30654","DOIUrl":"10.1002/jcb.30654","url":null,"abstract":"<p><p>Metastatic colorectal carcinoma (mCRC) is one of the prevalent subtypes of human cancers and is caused by the alterations of various lifestyle and diet-associated factors. β-catenin, GSK-3β, PI3K-α, AKT1, and NF-κB p50 are known to be the critical regulators of tumorigenesis and immunopathogenesis of mCRC. Unfortunately, current drugs have limited efficacy, side effects and can lead to chemoresistance. Therefore, searching for a nontoxic, efficacious anti-mCRC agent is crucial and of utmost interest. The present study demonstrates the identification of a productive and nontoxic anti-mCRC agent through a five-targets (β-catenin, GSK-3β, PI3K-α, AKT1, and p50)-based and three-tier (binding affinity, pharmacokinetics, and pharmacophore) screening strategy involving a series of 30 phytocompounds having a background of anti-inflammatory/anti-mCRC efficacy alongside 5-fluorouracil (FU), a reference drug. Luteolin (a phyto-flavonoid) was eventually rendered as the most potent and safe phytocompound. This inference was verified through three rounds of validation. Firstly, luteolin was found to be effective against the different mCRC cell lines (HCT-15, HCT-116, DLD-1, and HT-29) without hampering the viability of non-tumorigenic ones (RWPE-1). Secondly, luteolin was found to curtail the clonogenicity of CRC cells, and finally, it also disrupted the formation of colospheroids, a characteristic of metastasis. While studying the mechanistic insights, luteolin was found to inhibit β-catenin activity (a key regulator of mCRC) through direct physical interactions, promoting its degradation by activating GSK3-β and ceasing its activation by inactivating AKT1 and PI3K-α. Luteolin also inhibited p50 activity, which could be useful in mitigating mCRC-associated proinflammatory milieu. In conclusion, our study provides evidence on the efficacy of luteolin against the critical key regulators of immunopathogenesis of mCRC and recommends further studies in animal models to determine the effectiveness efficacy of this natural compound for treating mCRC in the future.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":" ","pages":"e30654"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142288028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Solasodine Downregulates ABCB1 Overexpression in Multidrug Resistant Cancer Cells Via Inhibiting Nrf2/Keap1 Signaling Pathway.","authors":"Pradhapsingh Bharathiraja, Sugumar Baskar, N Rajendra Prasad","doi":"10.1002/jcb.30674","DOIUrl":"10.1002/jcb.30674","url":null,"abstract":"<p><p>Multidrug-resistant (MDR) cancer cells maintain redox homeostasis to eliminate oxidative stress-mediated cell death. This study explores the effects of solasodine on regulating P-glycoprotein (P-gp) expression through the Nrf2/Keap1 signaling pathway and oxidative stress-induced sensitization of drug-resistant cancer cells to chemotherapeutics. Initially, the oxidative stress indicators such as intracellular ROS generation, the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) and gamma-H2AX (γ-H2AX) in the KBChR-8-5 drug-resistant cells were measured. Additionally, the protein expression levels of Nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap1), and ATP Binding Cassette Subfamily B Member 1 (ABCB1)/P-gp were measured at various concentrations of solasodine (1, 5, & 10 µM) through immunofluorescence and western blot analysis. The antioxidant activities in the KBChR-8-5 cells were assessed using established protocols. In this investigation, the treatment with solasodine and doxorubicin combination showed a notable increase in intracellular ROS generation in KBChR-8-5 cells. Furthermore, this combination treatment led to enhanced nuclear condensation, elevated levels of 8-OHdG, and increased γ-H2AX foci formation in the KBChR-8-5 cells. Solasodine treatment effectively inhibited the nuclear translocation of Nrf2 and activation of the ABCB1 gene, consequently preventing overexpression of P-gp in KBChR-8-5 cells. Additionally, the combination therapy increased the lipid peroxidation levels while simultaneously reducing the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and the levels of glutathione (GSH). These results demonstrated that solasodine disrupts redox balance, and overcomes drug resistance by downregulating P-gp via regulating Nrf2/Keap1 signaling pathway in MDR cancer cells.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":" ","pages":"e30674"},"PeriodicalIF":3.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}