Cell Biology International最新文献

{"title":"miR-6844/HSD17B13 Axis Contributes the Malignant Phenotype of Hepatocellular Carcinoma Cells","authors":"Li Liao,&nbsp;Qilin Yi,&nbsp;Zhen Zhao,&nbsp;Ming Xu,&nbsp;Tao Wu,&nbsp;Shuai Chen,&nbsp;Yu Liu","doi":"10.1002/cbin.70025","DOIUrl":"10.1002/cbin.70025","url":null,"abstract":"<div>\u0000 \u0000 <p>Hepatocellular carcinoma (HCC) is a prevalent form of primary liver cancer, and aberrant miRNAs expression significantly contributes to its progression. Although the abnormal expression of miR-6844 in HCC has been reported, its impact on the malignant phenotype of HCC cells and its potential mechanism remains unclear. In this study, we initially conducted a bioinformatics analysis to investigate the differential expression of miR-6844 in HCC tissues and its impact on patient prognosis. The association between miR-6844 expression levels and clinical characteristics of HCC patients was subsequently investigated by integrating data from clinical samples. Ultimately, the impact of miR-6844 on the malignant phenotype of HCC cells and the underlying mechanisms were examined through in vitro cellular experiments. The results showed that a high expression of miR-6844 in HCC, which was associated with poor prognosis and exhibited significant correlations with intrahepatic metastasis and clinical stage among patients. The upregulation of miR-6844 promoted the proliferation, migration, and invasion of HCC cells while suppressing apoptosis. Conversely, the downregulation of miR-6844 significantly attenuated the malignant phenotype of HCC cells. In addition, <i>HSD17B13</i> was identified as a target gene of miR-6844, and the overexpression of HSD17B13 partially counteracted the oncogenic effects induced by miR-6844 in HCC cells, otherwise the opposite. Taken together, the above results suggest that miR-6844 plays a regulatory role in the malignant phenotype of HCC cells through its targeting of HSD17B13.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"836-851"},"PeriodicalIF":3.3,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974618","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":"IL-17C-Mediated Upregulation of SMURF2 Induces Psoriatic Changes in Keratinocytes by Facilitating PPP6C Ubiquitination","authors":"Jingyi Mao,&nbsp;Xin Ma,&nbsp;Yuanyuan Sun,&nbsp;Wuqing Wang,&nbsp;Bin Li","doi":"10.1002/cbin.70024","DOIUrl":"10.1002/cbin.70024","url":null,"abstract":"<div>\u0000 \u0000 <p>Psoriasis, a persistent inflammatory skin condition, affects approximately 2%–3% of the world's population. Increased IL-17C levels are noted in psoriatic lesions, alongside IL-17's ability to diminish protein phosphatase 6 catalytic subunit (PPP6C) expression in keratinocytes. Additionally, SMAD-specific E3 ubiquitin protein ligase 2 (SMURF2) facilitates the degradation of specific substrates through ubiquitination. However, the precise mechanisms of action involving IL-17C, SMURF2, and PPP6C in psoriasis remain unclear. Therefore, this study aims to delve into how IL-17C, SMURF2, and PPP6C contribute to psoriasis development. A psoriasis mice model was established using 5% imiquimod cream. And the expression of IL-17C, SMURF2, and PPP6C was tested. Further, an investigation was conducted using experimental techniques such as CCK-8, flow cytometry, colony formation assay, ELISA, qRT-PCR, western blot assay, co-immunoprecipitation, and ubiquitination assays. Employing both lentiviral transfection and plasmid transfection methods, an in-depth investigation was conducted into the contributions of IL-17C, SMURF2, and PPP6C to psoriasis. The results showed that the IL-17C, Keratin 17 and SMURF2 were increased, and PPP6C was decreased in psoriasis mice model. Further, IL-17C enhanced the cell viability of human epidermal keratinocytes (HaCaT), induced inflammatory responses, and upregulated SMURF2 and Keratin 17 expression. When SMURF2 was silenced, the effects of IL-17C on HaCaT cells were significantly inhibited. Moreover, SMURF2 interacted with PPP6C, promoting its ubiquitination and degradation. Overexpression of SMURF2 further enhanced the effects of IL-17C on HaCaT cells by targeting PPP6C. In conclusion, our study uncovered the upregulation of SMURF2 mediated by IL-17C, leading to psoriasis-like alterations in keratinocytes through the promotion of PPP6C ubiquitination. This novel finding not only provides crucial insights into the molecular mechanisms of psoriasis but also offers potential avenues for innovative therapeutic strategies targeting this mechanism.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"798-809"},"PeriodicalIF":3.3,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974001","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":"Distribution of Troy (Tnfrsf19) in the Gastric Gland During Postnatal Development: Effects of Early Weaning","authors":"Isadora Campos Rattes,&nbsp;Kethleen Mesquita da Silva,&nbsp;Patrícia Gama","doi":"10.1002/cbin.70021","DOIUrl":"10.1002/cbin.70021","url":null,"abstract":"<p>This study investigates the distribution and role of the stem cell marker Troy (<i>Tnfrsf19</i>) in the gastric mucosa of rats during postnatal development and the effects of early weaning. Troy, previously identified as a reserve stem cell marker in adult gastric tissues, is examined across various developmental stages from birth to adulthood. We showed that Troy+ cells are scattered throughout the gastric gland in early postnatal stages, but they become concentrated in the basal portion of the gland as the rats mature. Additionally, early weaning affects Troy expression at its gene and protein levels, altering its distribution in the gastric mucosa. This suggests that early dietary changes may disrupt the organization and function of the secondary stem cell niche in the stomach, potentially impacting gastric gland homeostasis. We also used in silico analysis to compare the molecular functions of Troy+ zymogenic and parietal cells, finding distinct roles in proliferation and secretion. The results underscore the importance of Troy in gastric development and highlight the long-term impact of early weaning on gastric tissue organization and cell proliferation dynamics.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"772-784"},"PeriodicalIF":3.3,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810646","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":"Macrophage Protein Disulfide Isomerase Increases Infection by Leishmania amazonensis","authors":"Guilherme M. P. Carrara,&nbsp;Guilherme A. Souza-Silva,&nbsp;Tania C. B. d. Reis,&nbsp;Bruna C. d. Alencar,&nbsp;Silvia B. Boscardin,&nbsp;Peter E. Kima,&nbsp;Beatriz S. Stolf","doi":"10.1002/cbin.70020","DOIUrl":"10.1002/cbin.70020","url":null,"abstract":"<div>\u0000 \u0000 <p><i>Leishmania</i> spp. are protozoans with a digenetic life cycle responsible for causing tegumentary and visceral leishmaniasis. <i>Leishmania (L.) amazonensis</i> is the second most prevalent dermotropic species in Brazil. Infection in humans and other mammals takes place when phagocytes, mainly macrophages, uptake the parasite. Many proteins on the phagocytic cell surface participate in <i>Leishmania</i> phagocytosis. In this study, we evaluated the role of surface protein disulfide isomerase (PDI) in phagocytosis and infection of macrophages by <i>L. amazonensis</i>. PDI is the second most abundant chaperone in the endoplasmic reticulum. A unique study in the literature associated the presence of PDI on the macrophage surface with increased phagocytosis by <i>Leishmania (L.) infantum</i> (syn <i>L. chagasi</i>), the species most frequently associated with visceral leishmaniasis in the Americas. In the present work we evaluated <i>L. amazonensis</i> infections in transgenic FVB/NJ mice overexpressing PDI (TgPDIA1). We validated the presence of PDI on their macrophages surface by flow cytometry. We demonstrated that infection of macrophages pretreated with anti-PDI antibodies was lower compared to control cells. Accordingly, we showed that the overexpression of PDI increased the adhesion of parasites and infection of macrophages. We also demonstrated that macrophages overexpressing PDI internalize more zymosan particles. In vivo imaging of infections with luciferase-expressing parasites in wild-type and TgPDIA1 mice indicated that the overexpression of PDI was not associated with significant differences in footpad lesions and parasite burden, probably due to the ubiquitous overexpression of PDI and the roles of this molecule in other immune system functions.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"785-797"},"PeriodicalIF":3.3,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771393","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":"Induction of Ferroptosis by Shikonin in Gastric Cancer via the DLEU1/mTOR/GPX4 Axis","authors":"Yiying Wang,&nbsp;Midie Xu,&nbsp;Cheng Liu,&nbsp;Xin Wang,&nbsp;Xiaoyan Zhang,&nbsp;Weiqi Sheng,&nbsp;Xiaoyu Wang","doi":"10.1002/cbin.70018","DOIUrl":"10.1002/cbin.70018","url":null,"abstract":"<div>\u0000 \u0000 <p>Gastric cancer (GC) is the most prevalent cancer in Asia. Shikonin, one of the ingredients extracted from the roots of <i>Lithospermum erythrorhizon</i>, has been proven to be a necrosis inducer and has an antitumour effect on many cancers. We explored the mechanism of the antitumour effect of shikonin in GC. CCK8 and clonogenic assays were used to determine the effect of shikonin on the proliferation of GC cell lines. Shikonin could induce reactive oxygen species (ROS), lipid ROS, intracellular ferrous iron (Fe²⁺), and malondialdehyde (MDA) in GC. We also found that shikonin decreased the expression of GPX4 by suppressing GPX4 synthesis and decreasing ferritin. Furthermore, long noncoding RNA deleted in lymphocytic leukaemia 1 (DLEU1) is an oncogene in GC, and shikonin decreased DLEU1 expression in GC cells. Overexpression of DLEU1 eliminated the anticancer effect of shikonin. Mechanistically, shikonin might decrease GPX4 levels by inhibiting the DLEU1/mTOR pathway. DLEU1 was sponged with miR-9-3p, which also regulated mTOR and GPX4. A xenograft tumour model of GC was established, and shikonin treatment inhibited cell proliferation and induced ferroptosis. In conclusion, shikonin exerts its antitumour effects on GC by triggering ferroptosis, and the DLEU1/mTOR/GPX4 axis may play an essential role in shikonin-induced ferroptosis. Therefore, our findings provide a potential lead compound for treating GC.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 7","pages":"757-771"},"PeriodicalIF":3.3,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691284","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":"Identification of Potential Targets Associated With Programmed Cell Death for Acute Kidney Injury Based on WGCNA","authors":"Yu Wang,&nbsp;Bo Deng,&nbsp;Yu Pan,&nbsp;Feng Ding","doi":"10.1002/cbin.70019","DOIUrl":"10.1002/cbin.70019","url":null,"abstract":"<div>\u0000 \u0000 <p>Programmed cell death (PCD) pathways play a crucial role in maintaining normal cell turnover and tissue homeostasis, encompassing apoptosis and regulated necrosis. However, the involvement of PCD in the pathogenesis of acute kidney disease remains unexplored. In this study, we utilized gene expression profiling datasets (GSE139061) obtained from the Gene Expression Omnibus (GEO) database. Through differential gene expression analysis and weighted gene co-expression network analysis (WGCNA), we identified five key genes associated with PCD, namely <i>DPP4</i>, <i>ATF3</i>, <i>KIT</i>, <i>MSX1</i>, and <i>SNAI2</i> in acute kidney injury (AKI). Subsequently, single sample gene set enrichment analysis (ssGSEA) was employed to demonstrate the correlation between these five hub genes and immune cell infiltration as well as activation of immune pathways. Furthermore, we validated our findings by analyzing gene expression patterns using a mouse model of ischemia–reperfusion injury. In conclusion, our study is the first to propose the concept of PCD in the pathogenesis of AKI. This finding has significant implications for future investigations into pro-inflammatory immune mechanisms mediated by damage-associated molecular patterns (DAMPs) during the stages of AKI. Our findings underscore the necessity for further investigation into these molecules, which may offer new avenues for therapeutic intervention in AKI. These identified genes may serve as promising targets for intervention in cases of acute kidney diseases.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 6","pages":"723-735"},"PeriodicalIF":3.3,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668725","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":"Exposure of Bisphenols (BPA, BPB and BPC) in HepG2 Cells Results in Lysosomal Dysfunction and Lipid Accumulation","authors":"Kiran Gill,&nbsp;Eshika Bindal,&nbsp;Parul Garg,&nbsp;Deepak Kumar,&nbsp;Rajasri Bhattacharyya,&nbsp;Dibyajyoti Banerjee","doi":"10.1002/cbin.70017","DOIUrl":"10.1002/cbin.70017","url":null,"abstract":"<div>\u0000 \u0000 <p>Nonalcoholic fatty liver disease poses a significant public health concern, as do the issues surrounding plastic usage. The bisphenols are reported to cause fat accumulation in the liver. However, literature is scanty about the effect of bisphenols on lysosomes or lysosomal functions. We predicted the interaction of bisphenols with lysosomal proteins available in the online databases using in silico tools. Molecular docking revealed that chosen Bisphenols interact with critical lysosomal proteins including lipid hydrolyzing enzymes. Following exposure of BPA, BPB and BPC to HepG2 cells fat accumulation and lysosomal functions were evaluated. Exposure to BPB and BPC results intracellular fat accumulation under experimental conditions like BPA. All three Bisphenols disturb lysosomal homeostasis perhaps by different mechanisms. Overall our results suggest that Bisphenols can also cause fat accumulation in liver by disturbing lysosomal homeostasis.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 6","pages":"709-722"},"PeriodicalIF":3.3,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656291","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":"Piwei Peiyuan Prescription Attenuates the Progression of Chronic Atrophic Gastritis by Eliciting MAPK10-Mediated Mitochondrial Autophagy","authors":"Yi Zhang,&nbsp;Ying Wu,&nbsp;Bei Pei,&nbsp;Qin Sun,&nbsp;Cheng Zhang,&nbsp;Qi Yang,&nbsp;Yueping Jin,&nbsp;Jing Wu,&nbsp;Xuejun Li","doi":"10.1002/cbin.70016","DOIUrl":"10.1002/cbin.70016","url":null,"abstract":"<div>\u0000 \u0000 <p>Piwei Peiyuan (PWPY) prescription is a traditional Chinese medicine prescription and has been efficiently used in the clinics to treat chronic atrophic gastritis (CAG) for many years. However, the mechanism of action underlying PWPY for treating CAG remains elusive. A CAG rat animal and cell model was constructed in this study to explore the action mechanism of PWPY prescription in treating CAG. Here we show that PWPY attenuates the progression of CAG by eliciting MAPK10-mediated mitochondrial autophagy. Experimental model of CAG was introduced using <i>N</i>-methyl-n'-nitro-n-nitroguanidine (MNNG). Our histological analyses reveal that MNNG-induced CAG in rat undergoes classical morphological alterations judged by immunohistochemistry and serum level of PGⅠ, PGⅡ, and G17. Importantly, PWPY treatment prevents the progression of MNNG-induced CAG judged by serum level of PGⅠ, PGⅡ, and G17. Interestingly, PWPY treatment inhibits MAPK10 activity judged by biochemical assays and promotes mitochondrial autophagy judged by electron microscopic analyses. Thus, we conclude that PWPY attenuates the progression of MNNG-induced CAG and prevents precancerous lesions by harnessing MAPK10-elicited mitochondrial autophagy. The MNNG-induced experimental CAG model provides a robust platform for further delineating therapeutic targets underlying PWPY regimen.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 6","pages":"692-708"},"PeriodicalIF":3.3,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656296","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":"Cellular and Molecular Mechanisms of Phytochemicals Against Inflammation-Associated Diseases and Viral Infection","authors":"Zhaodi Zheng,&nbsp;Junying Gao,&nbsp;Yubing Ma,&nbsp;Xitan Hou","doi":"10.1002/cbin.70011","DOIUrl":"10.1002/cbin.70011","url":null,"abstract":"<div>\u0000 \u0000 <p>Inflammation-associated diseases have become widespread and pose a significant threat to human health, and the therapeutic methods for diverse diseases are inadequate due to the undesirable effects of synthetic ingredients. Recently, more and more evidence indicated that phytochemicals, plant secondary metabolites, have numerous therapeutic functions against human diseases via affecting a variety of mechanisms with their distinct advantages of high efficiency and low toxicity. Here, we highlight the mechanisms of phytochemicals to hinder inflammation-associated diseases (including Inflammatory diseases, cardiovascular diseases, metabolic syndrome, neurological disorders, skin diseases, respiratory diseases, kidney diseases, gastrointestinal diseases, retinal diseases, viral infections) by regulating the crosstalk among various signal cascades (including MicroRNAs, SIRT1, DNMTs, NF-κB, NLRP3, TGF-β, the Gasdermin-mediated pyroptosis pathway), which can be considered as a novel and potential therapeutic strategy. Furthermore, phytochemicals could prevent virus infection by disturbing different targets in the virus replication cycle. However, natural plants have shown limited bioavailability due to their low water solubility, the use of adjuvants such as liposomal phytochemicals, phytochemical nanoparticles and phytochemicals-phospholipid complex promote their bioavailability to exhibit beneficial effects against various diseases. The purpose of this review is to explore the molecular mechanisms and promising applications of phytochemicals in the fields of inflammation-associated diseases and virus infection to provide some direction.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 6","pages":"606-633"},"PeriodicalIF":3.3,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647470","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":"FLOT1 Is a Novel Serum Biomarker of Ovarian Cancer Targeted by N6-methyladenosine Modification Inhibition","authors":"Bin Guan,&nbsp;Qi Lu,&nbsp;Junyu Chen,&nbsp;Jingyi Fang,&nbsp;Zhenyu Liu,&nbsp;Wei Li,&nbsp;Lingyun Zhang,&nbsp;Guoxiong Xu","doi":"10.1002/cbin.70015","DOIUrl":"10.1002/cbin.70015","url":null,"abstract":"<p>Ovarian cancer (OC) is a deadly disease and lacks a precise marker for diagnosis worldwide. Our previous work has shown the overexpression of flotillin-1 (FLOT1) in OC tissue. To improve diagnostic sensitivity and accuracy, we evaluated the serum level of FLOT1 in OC patients and found that the serum concentration of FLOT1 as well as CA125 was significantly increased in patients with OC compared with healthy control (<i>p</i> &lt; 0.01) and those with benign tumors (<i>p</i> &lt; 0.05). The detection rate (above the upper limit of a cut-off value) of FLOT1 and CA125 was 77.78% and 72.22%, respectively, in patients with OC, which was increased to 88.89% in combination. The elevation of FLOT1 was confirmed in the serum of nude mice after the implantation of human OC cells. A high level of FLOT1 protein in the serum was positively correlated with the overexpression of FLOT1 protein in OC tissues. Furthermore, the level of m⁶A modification of FLOT1 mRNA was significantly high in OC cells compared with normal ovarian epithelial cells, leading to an increase in FLOT1 mRNA expression. Application of a methylation inhibitor, 3-deazaadenosine, decreased FLOT1 mRNA expression in OC cells and suppressed tumor formation in a xenograft mouse model. In conclusion, the current study demonstrated that FLOT1 is a novel serum biomarker of OC and can be targeted by m⁶A modification inhibition. These data highlight the potential application of FLOT1 as a diagnostic marker and a therapeutic target for patients with OC.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 6","pages":"674-691"},"PeriodicalIF":3.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596362","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}