Experimental cell research最新文献

{"title":"MiRNA29a-3p negatively regulates ISL1–Integrin β1 axis to suppress gastric cancer progression","authors":"Ziwei She ,&nbsp;Haosheng Dong ,&nbsp;Yang Li ,&nbsp;Ping Chen ,&nbsp;Chunyan Zhou ,&nbsp;Weiping Wang ,&nbsp;Zhuqing Jia ,&nbsp;Qiong Shi","doi":"10.1016/j.yexcr.2024.114288","DOIUrl":"10.1016/j.yexcr.2024.114288","url":null,"abstract":"<div><div>Insulin gene enhancer protein 1 (ISL1) belongs to the LIM homeodomain transcription factor family, which is closely related to the development of several cancers. We previously found that abnormally high ISL1 expression is involved in gastric cancer (GC) metastasis. However, the specific role of ISL1 and its regulatory mechanisms in GC metastasis warrant elucidation. In this study, we found that ISL1 is highly expressed in GC tissues and positively correlated with GC development, promoting cell migration and invasion <em>in vivo</em> and <em>in vitro</em>. Moreover, miRNA29a-3p can target ISL1 and thus inhibit GC cell migration. Furthermore, ISL1 upregulates ITGB1 by binding to its enhancer; nevertheless, ISL1–ITGB1 axis expression can be regulated using miRNA29a-3p. In GC cell nuclei, ISL1 and annexin A2 (ANXA2) form a transcriptional activator complex at the <em>ITGB1</em> enhancer, thus promoting ITGB1 expression. In GC cell cytoplasm, the ISL1–ANXA2 complex synergistically activates matrix metalloproteinases, thus promoting cell migration. In conclusion, ISL1 is a potential therapeutic target for GC.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 1","pages":"Article 114288"},"PeriodicalIF":3.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142555048","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":"Histone MARylation regulates lipid metabolism in colorectal cancer by promoting IGFBP1 methylation","authors":"Chuanling Wang ,&nbsp;Yi Tang ,&nbsp;ShuXian Zhang ,&nbsp;Ming Li ,&nbsp;QingShu Li ,&nbsp;Ming Xiao ,&nbsp;Lian Yang ,&nbsp;YaLan Wang","doi":"10.1016/j.yexcr.2024.114308","DOIUrl":"10.1016/j.yexcr.2024.114308","url":null,"abstract":"<div><div>In the global health community, colorectal cancer (CRC) is a major concern, with a high rate of incidence. Mono-ADP-ribosylation (MARylation) is a type of epigenetics and recognized as one of the causes of CRC development and progression. Although the modification level and target proteins in CRC remain unclear, it has been found that MARylation of arginine-117 of histone 3 (H3R117) promotes the proliferation, upregulates methylation of tumor suppressor gene, and is tightly associated with the metabolic processes in LoVo cells. Lipid metabolism disorder is involved in the development of CRC at the early stage. Our study revealed that MARylation of H3R117 of the LoVo cells modulated lipid metabolism, increased cholesterol synthesis, promoted lipid raft (LR) protein IGF-1R distribution, and inhibited cell apoptosis through IGFBP1. In addition, bioinformatics analyses revealed that IGFBP1 promoter was hypermethylated in CRC when compared to that in normal tissues. Moreover, H3R117 MARylation upregulated the methylation of IGFBP1 promoter through histone H3 citrullination (H3cit) by increasing the H3K9me2, heterochromatin protein1 (HP1), and DNA methyltransferase 1 (DNMT1) enrichment of IGFBP1 promoter. Accordingly, IGFBP1 may function as a tumor suppressor gene, while H3R117 MARylation may promote CRC development. Our study findings enrich the available data on epigenetics of CRC and provide a new idea and experimental basis for H3R117 MARylation as a target in CRC treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 1","pages":"Article 114308"},"PeriodicalIF":3.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142555047","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":"Knockdown of ANO1 decreases TGF-β- and IL-6-induced adhesion and migration of cardiac fibroblasts by inhibiting the expression of integrin and focal adhesion kinase","authors":"Xiangqin Tian ,&nbsp;Yajing Zhang ,&nbsp;Hezhe Gong ,&nbsp;Mengru Bai ,&nbsp;Changye Sun ,&nbsp;Yangyang Jia ,&nbsp;Changen Duan ,&nbsp;Xianwei Wang","doi":"10.1016/j.yexcr.2024.114321","DOIUrl":"10.1016/j.yexcr.2024.114321","url":null,"abstract":"<div><div>Ischemic cardiac injury triggers a significant inflammatory response, activating and mobilizing cardiac fibroblasts (CFs), which ultimately contributes to myocardial fibrosis. In this study, we investigated the role of ANO1, a calcium-activated chloride channel (CaCC) protein, in regulating CFs migration and adhesion under inflammatory conditions. Our results demonstrated that ANO1 knockdown significantly attenuated TGF-β- and IL-6-induced adhesion and migration of CFs. This inhibitory effect was mediated through the downregulation of integrin expression and reduced activation of focal adhesion kinase (FAK), key components in cellular adhesion and motility pathways. This study provides new insights into the mechanisms underlying CFs migration and adhesion, highlighting the potential of ANO1 as a therapeutic target for mitigating adverse fibrotic remodeling following myocardial infarction.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 1","pages":"Article 114321"},"PeriodicalIF":3.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589702","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":"Erratum to \"BRAFV600E promotes anchorage-independent growth but inhibits anchorage-dependent growth in hTERT/Cdk4-Immortalized normal human bronchial epithelial cells\" [Volume 439, June 2024, 114057].","authors":"Mitsuo Sato","doi":"10.1016/j.yexcr.2024.114290","DOIUrl":"10.1016/j.yexcr.2024.114290","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114290"},"PeriodicalIF":3.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617385","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":"PHLDA1 protects intestinal barrier function via restricting intestinal epithelial cells apoptosis in inflammatory bowel disease","authors":"Ziwei Zeng ,&nbsp;Yiming Shi ,&nbsp;Yonghua Cai ,&nbsp;Xin Yang ,&nbsp;Xiaobin Zheng ,&nbsp;Liang Huang ,&nbsp;Zhenxing Liang ,&nbsp;Zhanzhen Liu ,&nbsp;Shuangling Luo ,&nbsp;Li Xiong ,&nbsp;Shujuan Li ,&nbsp;Zhihang Liu ,&nbsp;Liang Kang ,&nbsp;Huashan Liu ,&nbsp;Wenxin Li","doi":"10.1016/j.yexcr.2024.114322","DOIUrl":"10.1016/j.yexcr.2024.114322","url":null,"abstract":"<div><div>The current approach to treating inflammatory bowel disease (IBD) primarily focuses on managing inflammation rather than maintaining the integrity of the intestinal barrier. In our study, we sought to investigate the potential role of PHLDA1 in preserving intestinal barrier function as a promising strategy for treating IBD. We observed a significant decrease in PHLDA1 expression in intestinal epithelial cells (IECs) of both IBD patients and mice with chemically induced colitis. This deficiency of PHLDA1 led to increased apoptosis of IECs, resulting in a compromised epithelial barrier and the invasion of commensal bacteria into the mucosa. Consequently, this microbial invasion substantially exacerbated colonic inflammation in mice with the specific knockout of PHLDA1 in IECs (Phlda1^IEC−KO) compared to their control littermates. Mechanistically, we found evidence of PHLDA1 interacting with MCL1 to protect against K48-linked polyubiquitylation at the K40 lysine residue, thus preventing ubiquitin-proteasome degradation through the MCL1 ubiquitin ligase E3 (Mule). We further confirmed that the PHLDA1-MCL1-Mule signaling pathway plays a critical role in the development of IBD. Notably, our study demonstrated that enhancing MCL1 levels or reducing Mule expression using adeno-associated virus (AAV) attenuated experimental colitis in Phlda1^IEC−KO mice. Collectively, our findings emphasize the significance of PHLDA1 in the pathogenesis of IBD and propose that targeting the PHLDA1-MCL1-Mule signaling pathway could be a viable approach for combating IBD.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 1","pages":"Article 114322"},"PeriodicalIF":3.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603326","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":"A human tissue-based model of renal inflammation","authors":"Camilla Merrild ,&nbsp;Gitte A. Pedersen ,&nbsp;Kristian W. Antonsen ,&nbsp;Mia G. Madsen ,&nbsp;Anna K. Keller ,&nbsp;Holger J. Møller ,&nbsp;Lene N. Nejsum ,&nbsp;Henricus A.M. Mutsaers ,&nbsp;Rikke Nørregaard","doi":"10.1016/j.yexcr.2024.114309","DOIUrl":"10.1016/j.yexcr.2024.114309","url":null,"abstract":"<div><div>Inflammation plays a key role in both the onset and progression of various kidney diseases. However, the specific molecular and cellular mechanisms by which inflammation drives kidney diseases from different etiologies remain to be elucidated. To enhance our understanding of these mechanisms, a reliable and translational human model of renal inflammation is needed.</div><div>Here, we aim to establish such a model using human precision-cut kidney slices (PCKS). The PCKS were prepared from fresh, macroscopically healthy kidney tissue and cultured for 3h–48h with or without tumor necrosis factor-α (TNFα), or its inhibitor Etanercept. The ensuing inflammatory response in the slices was evaluated using both qPCR and a cytokine array. Furthermore, the presence of immune cells was visualized using immunofluorescent staining, and the activation potential of tissue-resident macrophages was examined with ELISA.</div><div>We observed a culture-induced inflammatory response, reflected by increased expression of pro-inflammatory genes <em>TNF</em>, <em>IL1B</em>, <em>CCL2</em>, and <em>IL6</em>. This response could be partially inhibited by Etanercept, indicating that TNFα plays a role in the observed response. Moreover, we found that TNFα stimulation further increased the gene expression of <em>TNF</em>, <em>IL1B</em>, <em>CCL2</em>, and <em>IL6</em>, as well as the production of several chemokines and cytokines, including CXCL5, MCP1, MCP3, and IL-6. Lastly, we observed the presence of CD14- and HLA-DR-positive cells, as well as proliferating (CD68- and PCNA-positive) and activated macrophages in the slices during incubation. In conclusion, this study presents a novel human model for investigating renal inflammation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 1","pages":"Article 114309"},"PeriodicalIF":3.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544553","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":"Has_circ_0002360 facilitates immune evasion by enhancing heterogeneous nuclear ribonucleoprotein A1 stability, thereby promoting malignant progression in non-small cell lung cancer.","authors":"Jun Fan, Lei Xue, Rongxin Lu, Jinyuan Liu, Jinhua Luo","doi":"10.1016/j.yexcr.2024.114312","DOIUrl":"10.1016/j.yexcr.2024.114312","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) is marked by complex molecular aberrations including differential expression of circular RNAs (circRNAs). hsa_circ_0002360, a circRNA, has been identified as overexpressed in NSCLC. This study aimed to evaluate the expression patterns of hsa_circ_0002360 and its potential role as an oncogenic factor in NSCLC. We analyzed two GEO datasets (GSE112214 and GSE158695) using R software to identify differentially expressed circRNAs. Quantitative reverse transcription PCR (qRT-PCR) assessed the expression of hsa_circ_0002360 in NSCLC tissues and cell lines compared to controls. We used siRNA and overexpression vectors to modulate hsa_circ_0002360 levels in A549 cells, followed by assays to assess proliferation, migration, invasion, apoptosis, and epithelial-mesenchymal transition (EMT). Interactions with RNA-binding proteins, specifically HNRNPA1, were investigated using RNA-pull down and RIP assays. In GEO datasets GSE112214 and GSE158695, hsa_circ_0002360 was identified as significantly overexpressed in NSCLC, a finding supported by qRT-PCR analyses showing higher levels in NSCLC tissues and cell lines compared to controls. Functional assays demonstrated that knockdown of hsa_circ_0002360 in A549 cells decreased proliferation, migration, invasion, and altered epithelial-mesenchymal transition marker expression, while inducing apoptosis, suggesting its oncogenic role. Conversely, overexpression promoted tumor characteristics, corroborated by in vivo xenograft models showing increased tumor growth. Hsa_circ_0002360's interaction with HNRNPA1, evidenced through RNA-pull down and RIP assays, implicates it in regulatory pathways that enhance NSCLC progression. This expression was also correlated with advanced TNM stages and metastasis, highlighting its potential as a therapeutic target. hsa_circ_0002360 acts as an oncogene in NSCLC, promoting tumor progression and metastasis through regulation of cell growth, apoptosis, and EMT processes. The interaction between hsa_circ_0002360 and HNRNPA1 suggests a novel mechanism of circRNA-mediated modulation of NSCLC pathology, providing potential targets for therapeutic intervention.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114312"},"PeriodicalIF":3.3,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544555","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":"METTL14-mediated m6A methylation regulates pathological retinal neovascularization by targeting autophagy","authors":"Yang Yu ,&nbsp;Huiling Nie ,&nbsp;Xun Qin ,&nbsp;Xi Chen ,&nbsp;Xiumiao Li ,&nbsp;Jin Yao","doi":"10.1016/j.yexcr.2024.114291","DOIUrl":"10.1016/j.yexcr.2024.114291","url":null,"abstract":"<div><div>Pathological retinal neovascularization (RNV) is a prevalent characteristic of various ocular diseases, including proliferative diabetic retinopathy (PDR), retinopathy of prematurity (ROP), and retinal vein occlusion (RVO). While the importance of N6-methyladenosine (m6A) modification in diverse disease contexts is well-established, its functional role in pathological RNV remains unclear. Herein, we investigated the involvement of m6A modification and its core methyltransferase, METTL14, in a model of oxygen-induced retinopathy (OIR) to elucidate their contribution to retinal angiogenesis. In this study, we observed heightened levels of m6A modification and elevated expression of METTL14 in the OIR model, suggesting their potential implication in pathological RNV. Employing targeted knockdown of METTL14, we revealed that its depletion activated autophagy flux in human retinal vascular endothelial cells (HRVECs), consequently inhibiting the angiogenic capacity of endothelial cells. Mechanistically, we demonstrated that METTL14 exerts its regulatory influence on autophagy flux by modulating the stability of ATG7, a pivotal protein involved in autophagy. Specifically, METTL14 knockdown led to increased ATG7 expression at both mRNA and protein levels, accompanied by reduced m6A methylation of ATG7 mRNA and enhanced mRNA stability. Moreover, silencing of ATG7 counteracted the effects of METTL14 knockdown on endothelial cell functions, emphasizing ATG7 as a downstream target of METTL14-mediated autophagy in HRVECs. After all, our findings provide valuable insights into the pathogenesis of retinal pathological angiogenesis and potential therapeutic targets for the treatment of ocular neovascular diseases.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 1","pages":"Article 114291"},"PeriodicalIF":3.3,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497748","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":"Downregulation of heat shock protein 47 caused lysosomal dysfunction leading to excessive chondrocyte apoptosis","authors":"Yawen Shi ,&nbsp;Ying He ,&nbsp;Yanan Li ,&nbsp;Meng Zhang ,&nbsp;Yinan Liu ,&nbsp;Hui Wang ,&nbsp;Zhiran Shen ,&nbsp;Xiaoru Zhao ,&nbsp;Rui Wang ,&nbsp;Tianyou Ma ,&nbsp;Pinglin Yang ,&nbsp;Jinghong Chen","doi":"10.1016/j.yexcr.2024.114294","DOIUrl":"10.1016/j.yexcr.2024.114294","url":null,"abstract":"<div><div>Heat shock protein 47 (HSP47) is a collagen-specific chaperone present in several regions of the endoplasmic reticulum and cytoplasm. Elevated HSP47 expression in cells causes various cancers and fibrotic disorders. However, the consequences of HSP47 downregulation leading to chondrocyte death, as well as the underlying pathways, remain largely unclear. This study presents the first experimental evidence of the localization of HSP47 on lysosomes. Additionally, it successfully designed and generated shRNA HSP47 target sequences to suppress the expression of HSP47 in ATDC5 chondrocytes using lentiviral vectors. By employing a chondrocyte model that has undergone stable downregulation of HSP47, we observed that HSP47 downregulation in chondrocytes, disturbs the acidic homeostatic environment of chondrocyte lysosomes, causes hydrolytic enzyme activity dysregulation, impairs the lysosome-mediated autophagy-lysosome pathway, and causes abnormal expression of lysosomal morphology, number, and functional effector proteins. This implies the significance of the presence of HSP47 in maintaining proper lysosomal function. Significantly, the inhibitor CA-074 Me, which can restore the dysfunction of lysosomes, successfully reversed the negative effects of HSP47 on the autophagy-lysosomal pathway and partially reduced the occurrence of excessive cell death in chondrocytes. This suggests that maintaining proper lysosomal function is crucial for preventing HSP47-induced apoptosis in chondrocytes. The existence of HSP47 is crucial for preserving optimal lysosomal function and autophagic flux, while also inhibiting excessive apoptosis in ATDC5 chondrocytes.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 1","pages":"Article 114294"},"PeriodicalIF":3.3,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497749","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":"ALKBH5 promotes T-cell acute lymphoblastic leukemia growth via m⁶A-guided epigenetic inhibition of miR-20a-5p.","authors":"Jiazhuo Liu, Xin Zhang, Yi Liao, Chunlan Zhang, Leiwen Peng","doi":"10.1016/j.yexcr.2024.114293","DOIUrl":"https://doi.org/10.1016/j.yexcr.2024.114293","url":null,"abstract":"<p><p>This study investigates the role of ALKBH5-mediated m⁶A demethylation in T-cell acute lymphoblastic leukemia (T-ALL). T-ALL cell lines (HPB-ALL, MOLT4, Jurkat, CCRF-CEM) and human T cells were analyzed. CCRF-CEM and Jurkat cells were transfected with si-ALKBH5, miR-20a-5p-inhibitor, and pcDNA3.1-DDX5. The expression levels of ALKBH5, miR-20a-5p, and DDX5 in these cells were determined using qRT-PCR and Western blotting. Cell viability, proliferation, colony formation, and apoptosis were assessed using CCK-8, EdU staining, colony formation assay, and flow cytometry. mRNA m6A levels were quantified with an m6A RNA methylation detection reagent, and RNA immunoprecipitation was employed to measure the enrichment of DGCR8 and m6A on the primary transcript pri-miR-20a of miR-20a-5p. Dual-luciferase assay confirmed the binding relationship between miR-20a-5p and DDX5. Results showed that ALKBH5 and DDX5 were upregulated in T-ALL tissues and cells, whereas miR-20a-5p was downregulated. Silencing ALKBH5 inhibited T-ALL cell viability, colony formation, and proliferation, while promoting apoptosis. These effects were reversed by miR-20a-5p inhibition or DDX5 overexpression. ALKBH5 reduced the relative m⁶A level in T-ALL cells and decreased miR-20a-5p expression by reducing DGCR8 binding to pri-miR-20a-5p. miR-20a-5p suppressed DDX5 transcription. In conclusion, ALKBH5-mediated m⁶A demethylation decreases DGCR8 binding to pri-miR-20a, thereby repressing miR-20a-5p expression and enhancing DDX5 expression, ultimately inhibiting T-ALL cell apoptosis and promoting proliferation.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114293"},"PeriodicalIF":3.3,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497745","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}