Journal of cellular biochemistry最新文献

{"title":"Hypoxic Secretome and Exosomes Derived From Human Glioblastoma Cells (U87MG) Promote Protumorigenic Phenotype of Microglia in Vitro","authors":"Sangati Pancholi,&nbsp;Ritvi Shah,&nbsp;Utsav Bose,&nbsp;Ankit Yadav,&nbsp;Karthik Murukan,&nbsp;Prakash Pillai","doi":"10.1002/jcb.70002","DOIUrl":"https://doi.org/10.1002/jcb.70002","url":null,"abstract":"<div>\u0000 \u0000 <p>Glioblastoma multiforme (GBM), a highly heterogeneous CNS tumor known for its highest incidence rates and poor prognosis has shown limited success in the therapies due to hypoxia—driving immune-suppression in the tumor microenvironment (TME). Emerging evidence highlights the involvement of tumor cell-derived exosomes in tumor-associated microglia polarization via transfer of exosomal onco-proteins and miRNAs. Although the regulatory role of long noncoding RNAs (lncRNAs) in immune signaling are known, its mechanism in microglial polarization via exosomes in GBM still remains poorly understood. In our study, we found that in comparison to the normoxic GBM-derived exosomes lncRNA H19 was significantly upregulated in hypoxic GBM-derived exosomes. Hypoxic GBM-derived exosomes and secretome (conditioned media) caused the reduction in the % phagocytosis of microglia as compared with the control group. Moreover, GBM secretome caused increase in the M2-specific genes (IL10, STAT-3, CD163, CD206) in microglia indicating its polarization to the protumorigenic (M2) phenotype. LncRNA H19 knocked down GBM-secretome treatment in microglia further reduced the STAT-3 expression indicating H19 mediated signaling. Overall, our results suggest the involvement of hypoxic exosomes and lncRNA H19 in microglial polarization and H19 as a potential target.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 2","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143111512","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":"Proteasomal Dysfunction in Cancer: Mechanistic Pathways and Targeted Therapies","authors":"Pranit Hemant Bagde,&nbsp;Meenakshi Kandpal,&nbsp;Annu Rani,&nbsp;Sachin Kumar,&nbsp;Amit Mishra,&nbsp;Hem Chandra Jha","doi":"10.1002/jcb.70000","DOIUrl":"10.1002/jcb.70000","url":null,"abstract":"<div>\u0000 \u0000 <p>Proteasomes are the catalytic complexes in eukaryotic cells that decide the fate of proteins involved in various cellular processes in an energy-dependent manner. The proteasomal system performs its function by selectively destroying the proteins labelled with the small protein ubiquitin. Dysfunctional proteasomal activity is allegedly involved in various clinical disorders such as cancer, neurodegenerative disorders, ageing, and so forth, making it an important therapeutic target. Notably, compared to healthy cells, cancer cells have a higher protein homeostasis requirement and a faster protein turnover rate. The ubiquitin-proteasome system (UPS) helps cancer cells increase rapidly and experience less apoptotic cell death. Therefore, understanding UPS is essential to design and discover some effective inhibitors for cancer therapy. Hereby, we have focused on the role of the 26S proteasome complex, mainly the UPS, in carcinogenesis and seeking potential therapeutic targets in treating numerous cancers.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065853","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":"RETRACTION: Kaempferol Increases Apoptosis in Human Acute Promyelocytic Leukemia Cells and Inhibits Multidrug Resistance Genes","authors":"","doi":"10.1002/jcb.70001","DOIUrl":"10.1002/jcb.70001","url":null,"abstract":"<p><b>RETRACTION</b>: M. Moradzadeh, A. Tabarraei, H. R. Sadeghnia, A. Ghorbani, A. Mohamadkhani, S. Erfanian, and A. Sahebkar, “Kaempferol Increases Apoptosis in Human Acute Promyelocytic Leukemia Cells and Inhibits Multidrug Resistance Genes,” <i>Journal of Cellular Biochemistry</i> 119, no. 2 (2018): 2288–2297, https://doi.org/10.1002/jcb.26391.</p><p>The above article, published online on October 20, 2017 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed inappropriate image panel duplications between this article (Figure 5A,B) and other articles published by an overlapping group of authors, in which the images represent different experimental conditions. The explanation provided by the authors could not address these concerns. Thus, the editors have lost confidence in the presented data and consider the conclusions of this manuscript substantially compromised. A. Sahebkar disagrees with the retraction, the other co-authors remained unresponsive.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.70001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052713","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":"10.1002/jcb.30695","url":null,"abstract":"<p><b>RETRACTION:</b> S. Yang, J. Wang, W. Ge, and Y. Jiang, “Long Non-Coding RNA LOC554202 Promotes Laryngeal Squamous Cell Carcinoma Progression Through Regulating MiR-31,” <i>Journal of Cellular Biochemistry</i> 119, no. 8 (2018): 6953–6960, https://doi.org/10.1002/jcb.26902.</p><p>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":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30695","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mcl-1 is a Gatekeeper Molecule to Regulate the Crosstalk Between Ferroptotic Agent-Induced ER Stress and TRAIL-Induced Apoptosis","authors":"Young-Sun Lee,&nbsp;Farzaneh Vafaeinik,&nbsp;Lila Mouakkad,&nbsp;Dong-Hyun Kim,&nbsp;Xinxin Song,&nbsp;Lin Zhang,&nbsp;Yong J. Lee","doi":"10.1002/jcb.30681","DOIUrl":"10.1002/jcb.30681","url":null,"abstract":"<div>\u0000 \u0000 <p>We previously reported that ferroptosis interplays with apoptosis through the integration of two independent pathways: the endoplasmic reticulum (ER) stress signaling pathway and the mitochondria-dependent apoptotic signaling pathway. In this study, we investigated a potential gatekeeper molecule, Mcl-1, between the two signal transduction pathways. Morphology studies and cell death analyses confirmed that a combination treatment of ferroptotic agent erastin (ERA) and apoptotic agent TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) synergistically enhances TRAIL-induced apoptosis in human pancreatic adenocarcinoma BxPC3 and human colorectal carcinoma HCT116 cells. We further observed that ERA upregulated the proapoptotic proteins PUMA (p53 upregulated modulator of apoptosis) and NOXA, as well as the anti-apoptotic protein Mcl-1 (myeloid cell leukemia sequence 1). These results suggest that ERA upregulates these molecules which results in maintenance of the balance between them. Interestingly, this balance was offset when BxPC3 cells and HCT116 cells were treated with ERA in combination with TRAIL. Our studies suggest that the imbalance between PUMA and NOXA and Mcl-1 during the combined treatment is responsible for ERA-enhanced TRAIL-induced apoptosis. This hypothesis was tested by employing a HCT116 Mcl-1 knock-in of phosphorylation site mutant (S121A/E125A/S159A/T163A) and investigated the synergistic interaction between the ERA and TRAIL. Along with morphology and cell death studies, immunoblotting analyses revealed that HCT116 Mcl-1 knock-in mutant cells effectively inhibited reduction of Mcl-1 and apoptosis promoted by the combination treatment. Moreover, ERA enhanced Mcl-1 inhibitor-induced apoptosis. Collectively, our studies suggest that Mcl-1 is a gatekeeper molecule between the ER stress pathway and the mitochondria-dependent apoptotic pathway.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059173","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":"Recent Insights Into Wnt-Related tRNA-Derived Fragments (tRFs) in Human Diseases","authors":"Jinze Shen,&nbsp;Qurui Wang,&nbsp;Qinyuan Huang,&nbsp;Xiaowei Ying,&nbsp;Zehua Wang,&nbsp;Zhengfeng Xu,&nbsp;Jingyin Dong,&nbsp;Shiwei Duan","doi":"10.1002/jcb.30702","DOIUrl":"10.1002/jcb.30702","url":null,"abstract":"<div>\u0000 \u0000 <p>tRNA-derived fragments (tRFs) are a newly recognized class of small noncoding RNAs (sncRNAs) that play significant roles in various diseases. The Wnt pathway plays a key role in various physiological processes such as embryonic development, tissue renewal and regeneration. In the regulation of Wnt/β-catenin, Forkhead box k1(<i>FOXK1</i>), Frizzled class receptor 3 (<i>FZD3</i>), and <i>Wnt5b</i> can be targeted and inhibited by three tRFs: tRF3008A targets <i>FOXK1</i> to inhibit colorectal cancer (CRC), 5′-tiRNAVal targets <i>FZD3</i> to inhibit breast cancer (BrC), and tRF-22-8BWS7K092 targets <i>Wnt5b</i> to induce ferroptosis in lung cells. Additionally, tRF-24-V29K9UV3IU can inhibit the levels of FZD3, Van Gogh-like protein 1 (VANGL1), and cyclin D2 (CCND2) through an unexplained mechanism and play a role in inhibiting gastric cancer (GC). Clinical data has shown that the expression levels of certain tRFs are associated with the prognosis and pathological features of CRC and BrC patients. Low expression of tRF3008A is associated with poor prognosis and adverse pathological features in CRC patients, while high expression of tiRNA-Phe-GAA-003 and low expression of 5′-tiRNAVal are associated with poor prognosis and adverse pathological features in BrC patients. KEGG analysis has also shown that a variety of tRFs are involved in regulating the Wnt pathway and have been shown to play a role in a variety of diseases. For example, high expression of tRF-Gly-CCC-039 is associated with poor healing of diabetic foot, low expression of tsRNA-10277 is associated with high incidence of steroid-induced osteonecrosis of the femoral head (SONFH), high expression of tRF-22-8BWS7K092 is correlated with the severity of acute lung injury (ALI), and low expression of tsRNA-21109 is associated with the severity of systemic lupus erythematosus (SLE), and high expression of tRF-36-F900BY4D-84KRIME and tRF-23-87R8WP9IY, as well as low expression of tRF-40-86J8WPMN1E8Y7Z2R, were associated with high incidence of varicose vein (VV), and high expression of ts-34, was associated with high mortality of BrC. This article summarizes the biological function and mechanism of tRFs related to the Wnt pathway in cancer and other diseases, providing a new direction for subsequent translational medical research.</p></div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006135","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":"Gengnianchun Against H2O2-Induced Oxidative Damage in KGN Cells via miR-548m/FOXO3 Signaling","authors":"Jun Li,&nbsp;Yanqiu Rao,&nbsp;Tao Pu,&nbsp;Ting Xu,&nbsp;Wenjun Wang","doi":"10.1002/jcb.30701","DOIUrl":"10.1002/jcb.30701","url":null,"abstract":"<div>\u0000 \u0000 <p>Gengnianchun (GNC) is a traditional remedy used for diminished ovarian reserve, but its underlying mechanisms remain unclear. This study aimed to explore these mechanisms in human granulosa-like cancer (KGN) cells pretreated with medicated rat serum (MRS) before H₂O₂ exposure. MRS pretreatment significantly alleviated H₂O₂-induced cell damage, including improvements in cell viability, superoxide dismutase and GSH-Px activities, and Bcl-2 expression. Conversely, H₂O₂ treatment increased apoptosis, autophagosomes, IL-1β, TNF-α, reactive oxygen species, malondialdehyde levels, and the expression of LC-II/LC3-I, Bax, and Beclin-1. GEO database analysis revealed significant differential expression of several miRNAs, including miR-548m. qPCR confirmed that MRS upregulated miR-548m expression, which was downregulated by H₂O₂ in a dose-dependent manner. Preincubation with MRS prevented the decline in miR-548m expression and mitigated H₂O₂-induced damage, including improvements in cell viability, apoptosis, autophagy, and oxidative stress. miR-548m suppressed FOXO3 3'-UTR luciferase activity, and anti-miR-548m enhanced it. Transfection with miR-548m reduced FOXO3 mRNA and protein levels, while anti-miR-548m increased them. These findings suggest that GNC protects against H₂O₂-induced ovarian damage by modulating the miR-548m/FOXO3 axis, triggering autophagy and apoptosis.</p>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949513","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":"10.1002/jcb.30700","url":null,"abstract":"<p><b>NOTIFICATION:</b> Y.-C. Li, Y. Wang, D.-D. Li, Y. Zhang, T.-C. Zhao, and C.-F. Li, “Procaine Is a Specific DNA Methylation Inhibitor With Anti-Tumor Effect for Human Gastric Cancer,” <i>Journal of Cellular Biochemistry</i> 119, no. 2 (2018): 2440–2449, https://doi.org/10.1002/jcb.26407.</p><p>This notification is for the above article, published online on September 19, 2017 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Christian Behl; and Wiley Periodicals LLC. This notification has been issued in response to concerns raised by third parties [<span>1</span>]. The article references the non-verifiable cell line identifier “GSE-1” and the verified identifier “GES-1,” purportedly to refer to the same cell line. As the authors could not be reached to clarify this discrepancy, the journal has decided to publish this notification to inform and alert readers.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcb.30700","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural Dynamics of Neutral Amino Acid Transporter SLC6A19 in Simple and Complex Lipid Bilayers","authors":"Budheswar Dehury,&nbsp;Sarbani Mishra,&nbsp;Sunita Panda,&nbsp;Mahender Kumar Singh,&nbsp;Nischal L. Simha,&nbsp;Sanghamitra Pati","doi":"10.1002/jcb.30693","DOIUrl":"10.1002/jcb.30693","url":null,"abstract":"<p>B0AT1 (SLC6A19) is a major sodium-coupled neutral amino acid transporter that relies on angiotensin converting enzyme 2 (ACE2) or collectrin for membrane trafficking. Despite its significant role in disorders associated with amino acid metabolism, there is a deficit of comprehensive structure-function understanding of B0AT1 in lipid environment. Herein, we have employed molecular dynamics (MD) simulations to explore the architectural characteristics of B0AT1 in two distinct environments: a simplified POPC bilayer and a complex lipid system replicating the native membrane composition. Notably, our B0AT1 analysis in terms of structural stability and regions of maximum flexibility shows consistency in both the systems with enhanced structural features in the case of complex lipid system. Our findings suggest that diacylglycerol phospholipids significantly alter the pore radius, hydrophobic index, and surface charge distribution of B0AT1, thereby affecting the flexibility of transmembrane helices TM7, TM12, and loop connecting TM7-TM8, crucial for ACE2-B0AT1 interaction. Pro41, Ser190, Arg214, Arg240, Ser413, Pro414, Cys463, and Val582 are among the most prominent lipid binding residues that might influence B0AT1 functionality. We also perceive notable lipid mediated deviation in the degree of tilt and loss of helicity in TM1 and TM6 which might affect the substrate binding sites S1 and S2 in B0AT1. Considerably, destabilization in the structure of B0AT1 in lipid environment was evident upon mutation in TM domain, associated with Hartnup disorder through various structure-based protein stability tools. Our two-tiered approach allowed us to validate the use of POPC as a baseline for initial analyses of SLC transporters. Altogether, our all-atoms MD study provides a platform for future investigations into the structure-function mechanism of B0AT1 in realistic lipid mimetic bilayers and offers a framework for developing new therapeutic agents targeting this transporter.</p>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11696832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921830","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":"Supervillin-Mediated ZO-1 Downregulation Facilitates Migration of Cisplatin-Resistant HCT116 Colorectal Cancer Cells","authors":"Yali Hong,&nbsp;Xu Li,&nbsp;Rongchen Mao,&nbsp;Feier Zhou,&nbsp;Shengnan Li,&nbsp;Chao Zhu,&nbsp;Lai Jin","doi":"10.1002/jcb.30699","DOIUrl":"10.1002/jcb.30699","url":null,"abstract":"<div>\u0000 \u0000 <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>\u0000 </div>","PeriodicalId":15219,"journal":{"name":"Journal of cellular biochemistry","volume":"126 1","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-01-02","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}