Cell Division细胞分裂
Cell Division(英文缩写 CELL DIV),ISSN 1747-1028,eISSN 1747-1028,中文译名:细胞分裂 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
Cell Division 最新收录文献
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1. NSUN2 regulates PARP9 progression through m5C modification to mediate breast cancer progression.
PMID:日期:2026-07-19m5C modification plays a vital role in the progression of human cancers, including breast cancer (BC), but the function of NOP2/Sun RNA methyltransferase 2 (NSUN2), an RNA m5C modification enzyme, remains largely unclear. qRT-PCR, western blot and IHC assays were carried out to determine the expression of NSUN2, poly (ADP-ribose) polymerase 1 (PARP9) and Y box binding protein 1 (YBX1). EdU, flow cytometry, transwell, tube formation and sphere formation assays were conducted to evaluate cell proliferation, apoptosis, invasion, angiogenesis and stemness, respectively. ELISA was performed to examine the concentrations of inflammatory factors. RIP and pull-down assays were used to verify the interaction between NSUN2/YBX1 and PARP9. Murine xenograft model was constructed to explore the functions of NSUN2 and PARP9 in tumor growth in vivo. PARP9 silencing suppressed the proliferation, invasion, angiogenesis, stemness and immune escape, and promoted apoptosis in BC cells in vitro. Mechanically, NSUN2 functioned as an m5C writer that catalyzed m5C modification of PARP9 mRNA, while YBX1 acted as an m5C reader that recognized the modified transcript and enhanced its stability, thereby elevating PARP9 expression in BC cells. YBX1 could elevate PARP9 expression in BC cells. Moreover, NSUN2 knockdown restrained the malignant behaviors of BC cells, with PARP9 overexpression restored the effects. In addition, NSUN2 knockdown blocked tumorigenesis in vivo by regulating PARP9 expression. NSUN2-mediated m5C modification stabilizes PARP9 mRNA and is associated with enhanced BC progression and immune escape. The results broadened our understanding of the pathogenic mechanism of BC.
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2. The roles and clinical significance of LINC01140 in human cancers in the real world.
PMID:日期:2026-07-05Carcinogenic factors facilitate cell carcinogenesis and the progression of cancer. In contrast, tumor suppressor factors inhibit abnormal cell proliferation and cancer development. Accumulating evidence indicates that long non-coding RNAs (lncRNAs) can either suppress or promote cancer initiation and progression. LINC01140, a recently identified lncRNA, exhibits abnormal expression in cancerous tissues. Downstream target genes can be regulated, directly or indirectly, via miRNAs (miR-452-5p, miR-139-5p, miR-140-5p, miR-33a, miR-4742-5p, miR-200b-3p, and miR-452-5p), functioning as either oncogenes or tumor suppressors and contributing to cancer progression. Dysregulated LINC01140 expression shows significant correlations with patient survival, diagnosis, and cancer stage. Consequently, this review aims to examine the expression patterns, functional roles, and clinical significance of LINC01140 across pan-cancer, highlighting it as a potential therapeutic target for cancer treatment.
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3. Transcription factor FOXA1 suppresses ferroptosis of cervical cancer cells by upregulating SLC7A11 expression.
PMID:日期:2026-06-25Ferroptosis, a unique modality of cell death, possesses critical activity in tumorigenesis. This study defined the role of transcription factor (TF) forkhead box A1 (FOXA1) in modulating ferroptosis of cervical cancer (CC), a prevalent disease with high mortality rates in females. mRNA analysis was done by quantitative real-time PCR (qRT-PCR), and protein expression was analyzed by immunoblotting and immunohistochemistry (IHC). Colony formation and EdU proliferation assays were used to evaluate cell growth. Apoptosis was detected by flow cytometry. The contents of SOD, MDA, GSH, ROS and Fe were measured by assay kits. Chromatin immunoprecipitation (ChIP)-qPCR and luciferase assays were applied to analyzed the binding of FOXA1 to the SLC7A11 promoter. FOXA1 was an overexpressed factor in CC, which was related to prognosis of human CC. FOXA1 downregulation impaired CC cell in vitro proliferation, promoted apoptosis, and induced ferroptosis. FOXA1 was validated to bind to the promoter of SLC7A11 and enhance SLC7A11 transcription. Furthermore, the FOXA1/SLC7A11 cascade affected proliferation, apoptosis and ferroptosis of CC cells. In addition, FOXA1 downregulation impeded the in vivo tumorigenesis of C33A CC cells. Our study has identified FOXA1 as a crucial repressor of CC cell ferroptosis depending on its activation of SLC7A11 transcription. Developing inhibitors of FOXA1 is a promising way of harnessing ferroptosis for CC treatment.
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4. p53 overexpression counteracts the pro-survival effect of Bcl-2 by restoring MAMs function in cutaneous squamous cell carcinoma.
PMID:日期:2026-06-11Cutaneous squamous cell carcinoma (cSCC) is a prevalent type of skin cancer, and its development is strongly associated with impaired regulation of apoptosis. The anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and the tumor suppressor p53 play pivotal roles in controlling apoptotic signaling. Although Bcl-2 expression in cSCC has been reported to be heterogeneous, its role in mitochondria-associated membranes (MAMs)-mediated apoptosis remains unclear. This study aims to clarify how Bcl-2 and p53 regulate cSCC cell apoptosis by modulating the structure and function of MAMs. We constructed stable Bcl-2 overexpression (oe-Bcl-2) and Bcl-2/p53 co-overexpression (oe-Bcl-2 + oe-p53) A431 cell lines using lentiviral transduction. Transcriptome sequencing (RNA-seq) was performed, followed by pathway enrichment and protein-protein interaction (PPI) network analyses to screen for critical signaling routes. Cell apoptosis, growth, migratory capacity, and invasive potential were evaluated using flow cytometry, CCK-8, EdU incorporation, colony formation, and Transwell-based assays. Key MAMs functions, including Ca flux, mitochondrial membrane potential (MMP), ROS, and ATP levels, were measured. Subcutaneous tumor models in nude mice were used for in vivo validation. RNA-seq analysis revealed that Bcl-2 regulates multiple apoptosis- and calcium signaling-related pathways, significantly affecting key MAM-associated proteins, including VDAC2, IP3R, SERCA2, as well as the p53 signaling pathway. Bcl-2 overexpression markedly enhanced proliferation and migration of A431 cells while reducing apoptosis. It also modulated mitochondrial membrane potential, ATP production, and ROS generation, suggesting that Bcl-2 exerts anti-apoptotic effects through MAMs. In contrast, Bcl-2 knockdown significantly suppressed proliferation and invasion while inducing apoptosis in A431 cells, further supporting its oncogenic role. Notably, p53 overexpression reversed these effects and significantly inhibited tumor growth in vivo. Our findings demonstrate that Bcl-2 promotes cSCC progression by modulating MAMs structure and function to inhibit p53-mediated mitochondrial apoptosis. The study identifies the novel Bcl-2-MAMs-p53 signaling axis that plays a pivotal role in determining cSCC cell fate, highlighting a promising target for therapeutic intervention.
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5. Esculentoside A suppresses the malignant progression of hepatocellular carcinoma by promoting RORB.
5. Esculentoside A通过促进RORB抑制肝细胞癌的恶性进展PMID:日期:2026-06-03Hepatocellular carcinoma (HCC) is a highly aggressive disease associated with a poor prognosis. The present study attempts to discover the potential of esculentoside A (EsA) in inhibiting HCC progression. Cell viability was assessed using the Cell Counting Kit-8 assays. At the same time, stemness and malignant behaviors were evaluated through sphere formation, Western blot (WB), flow cytometry, colony formation assays, and TUNEL. EsA treatment suppressed HCC cell proliferation, migration, invasion, and stemness in vitro and tumor growth in vivo. Bioinformatics identified retinoic acid receptor-related orphan receptor beta (RORB) as a potential target of EsA, and EsA induced RORB expression in HCC cells. EsA also inhibited Wnt signaling activity, as shown by TOP/FOP Flash assays and WB. Knockdown of RORB through lentivirus infection reversed the effects of EsA. At the same time, Wnt pathway inhibitor rescued the promotive role of RORB knockdown in HCC malignant behaviors, suggesting that EsA inhibited HCC progression via the RORB/Wnt axis. RORB expression was reduced and associated with higher Wnt signaling in tumor tissues from patients with HCC, and low RORB expression showed significant correlation with higher TNM staging in HCC patients. This study offers novel insights into the molecular mechanism of EsA in HCC.
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6. Linalool targets NR3C2 to inhibit NF-κB-mediated gastric cancer progression.
PMID:日期:2026-05-18Gastric cancer (GC) is a major global health challenge. This study explores the efficacy of linalool in GC and further elucidates its underlying mechanisms. Linalool inhibited the proliferation, migration, and invasion of GC cells and prevented transplanted tumor growth in nude mice. Linalool directly interacted with and stabilized the NR3C2 protein, inhibiting its proteasomal degradation. Functional rescue experiments demonstrated that knockdown of NR3C2 partially reversed the antitumor effects of linalool. Further studies revealed that NR3C2 transcriptionally activated NFKBIZ and inhibited NF-κB signaling, and restoring NFKBIZ expression reversed GC progression caused by NR3C2 deficiency. In clinical samples, the expression levels of NR3C2 and NFKBIZ were lower in GC tissues than in adjacent normal tissues, and the two markers were positively correlated in the tumor tissues. Furthermore, low expression of both NR3C2 and NFKBIZ was significantly associated with higher T stages and more advanced pTNM stages and was accompanied by NF-κB signaling activation and elevated levels of inflammatory cytokines in tumor tissues. Overall, linalool inhibits GC progression by upregulating NR3C2 and transcriptionally activating NFKBIZ, thereby suppressing NF-κB signaling. Low NR3C2/NFKBIZ expression is associated with adverse clinical and pathological features in GC.
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7. The adipogenesis-related gene CEBPD as a prognostic biomarker and functional tumor suppressor in breast cancer.
PMID:日期:2026-05-13This study explores the role of adipogenesis-related genes (ARGs) in breast cancer, focusing on CEBPD, a key gene linked to adipogenesis. Using the TCGA-BRCA dataset, differentially expressed ARGs (DARGs) were identified, revealing 26 upregulated and 57 downregulated genes. CEBPD emerged as a central prognostic gene, exhibiting significantly lower expression in tumor tissues, which correlated with poor survival outcomes, making it an independent prognostic indicator. A nomogram integrating CEBPD expression was developed to predict 1-year, 3-year, and 5-year survival with moderate accuracy. Functional validation in vitro confirmed that CEBPD expression was downregulated at mRNA levels in breast cancer. Enforced overexpression of CEBPD significantly suppressed cancer cell proliferation. Gene Set Variation Analysis (GSVA) highlighted significant associations between CEBPD and biological processes such as angiogenesis, apoptosis, hypoxia, and inflammation. Immune microenvironment analysis showed distinct patterns of immune cell infiltration based on CEBPD expression levels. Overall, CEBPD significantly influences breast cancer progression and patient prognosis, suggesting its potential as a biomarker for therapeutic strategies.
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8. PTTG1-mediated the transcription of c-myc promotes retinoblastoma progression.
PMID:日期:2026-04-29The oncogenic potential of pituitary tumor-transforming gene-1 (PTTG1) has been well-documented in multiple cancer types. This study explored the biological role and molecular mechanism of PTTG1 in retinoblastoma. PTTG1 and c-myc expression levels were assessed through RT-qPCR and western blot analysis. Y79 and SO-RB-50 cells underwent PTTG1 knockdown or c-myc overexpression treatment. Cell proliferation was evaluated using CCK-8 assay and colony formation experiments. Flow cytometry was utilized to analyze cell cycle progression and apoptosis. Western blotting was performed to determine the expression of cell apoptosis and cell cycle-related proteins. Functional rescue experiments were conducted to investigate the impact of c-myc on the malignant behaviors of RB cells. PTTG1 expression was found to be upregulated in retinoblastoma tissues compared to normal retinal samples. Silencing of PTTG1 resulted in decreased proliferation and colony formation ability of retinoblastoma cells, as well as the induction of apoptosis and cell cycle arrest. Additionally, downregulation of PTTG1 led to inhibition of c-myc, resulting in reduced levels of cyclin A, cyclin D1, CDK2, and CDK4. The overexpression of c-myc reversed the effects caused by silencing PTTG1 on malignant behaviors of retinoblastoma cells. PTTG1 promotes retinoblastoma cell proliferation and inhibits apoptosis via activating c-myc, which represents a potential value of PTTG1 for retinoblastoma treatment.
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9. Role of cadherin gene dysregulation in WNT signaling and nasopharyngeal carcinoma.
PMID:日期:2026-04-28Nasopharyngeal carcinoma (NPC) is a malignancy associated with genetic alterations and tumor progression. Cadherin genes (CDH1, CDH2, and CDH3) play key roles in cell adhesion, migration, and tissue integrity, and their role in NPC remains underexplored. This study investigates the expression, mutation patterns, and prognostic significance of cadherin genes in NPC. Eight normal nasal cell lines and six NPC cell lines were cultured. Gene expression was analyzed using RT-qPCR and validated using GSCA and HPA databases. Promoter methylation, mutation, and CNV analyses were conducted using OncoDB and cBioPortal. Gene knockdown experiments were performed in 5-8 F NPC cells using siRNA targeting CDH1, CDH2, and CDH3, followed by cell proliferation, colony formation, and wound healing assays. CDH1, CDH2, and CDH3 were significantly upregulated in NPC cell lines, and high expression correlated with poor prognosis. Mutational analysis revealed mutations in 100% of HNSC or NPC samples, with CDH3 showing the highest mutation rate (44%). CNV analysis showed amplifications in cadherin gene regions. Knockdown of cadherin genes in 5-8 F and C666-1 cells significantly reduced cell proliferation, colony formation, and migration. Additionally, Cadherin gene knockdown upregulated AXIN1 and WNT3A, indicating involvement in the WNT signaling pathway. Cadherin genes are upregulated in NPC, associated with poor prognosis, and regulate key cancer-related processes. They represent potential diagnostic, prognostic, and therapeutic targets for NPC.
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10. Overexpression of ENDOD1 inhibits proliferation, migration, and invasion of colorectal cancer.
PMID:日期:2026-04-26OBJECTIVE: This study aimed to investigate the biological function and the molecular mechanism of ENDOD1 in colorectal cancer (CRC) progression. METHODS: CRC-related differentially expressed genes (DEGs) were screened by analyzing GEO datasets (GSE41657, GSE8671, GSE41328, and GSE75548). The differential expression of ENDOD1 within human CRC cell lines (HCT116, HT-29, SW620, and SW480) versus human normal colonic epithelial cells (NCM460) was validated using RT-qPCR and Western blot. ENDOD1 overexpression vector and siRNA were constructed and transfected into HT29 cells. CCK-8, flow cytometry, scratch test, and Transwell assays were performed to assess HT29 cell viability, apoptosis, and migratory and invasive abilities. The regulatory role of ENDOD1 in tumor growth in vivo was investigated using a xenograft mouse model. Moreover, a Western blot was performed to determine Wnt/β-catenin signaling activation. RESULTS: ENDOD1 was down-regulated in CRC tissues of GSE41657, GSE8671, GSE41328, and GSE75548 datasets, as well as in CRC cell lines. ENDOD1 overexpression promoted HT29 cell apoptosis and suppressed cell viability, migration, and invasion; ENDOD1 downregulation suppressed HT29 cell apoptosis and enhanced cell viability, migration, and invasion. In vivo, ENDOD1 overexpression inhibited tumor growth, suppressed Ki67 expression, and promoted apoptosis in transplanted tumors in mice. Moreover, EMDOD1 overexpression was blocked, while ENDOD1 inhibition promoted the activation of the Wnt/β-catenin pathway. Pharmacological activation of the Wnt/β‑catenin pathway partially attenuated ENDOD1-mediated suppression in CRC cells. CONCLUSION: ENDOD1 expression level is decreased in CRC, and overexpression of ENDOD1 induces apoptosis, represses cell proliferation, migratory and invasive ability, and inhibits the Wnt/β-catenin signaling activation within CRC cells.