Ask about this productRelated genes to: E2F1 antibody
- Gene:
- E2F1 NIH gene
- Name:
- E2F transcription factor 1
- Previous symbol:
- RBBP3
- Synonyms:
- RBP3
- Chromosome:
- 20q11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-29
- Date modifiied:
- 2016-10-05
Related products to: E2F1 antibody
Related articles to: E2F1 antibody
- Background and objectivesWilms tumor, a common childhood malignancy, has been hypothesized to be associated with environmental factors such as formaldehyde exposure. As a potential endocrine disruptor with reported pro-proliferative effects, the molecular mechanism underlying the role of formaldehyde in Wilms tumor remains unclear. This study systematically investigated the mechanisms linking formaldehyde exposure to Wilms tumor using network toxicology and transcriptomic analysis.MethodsTranscriptomic data were obtained from The Cancer Genome Atlas and Gene Expression Omnibus databases, whereas formaldehyde-related targets were predicted using the Search Tool for Interactions of Chemicals and Comparative Toxicogenomics databases. Candidate genes were screened through differential expression (|log2FC| > 2.5, < 0.05) and weighted gene coexpression network analyses. Prognostic key genes were identified using univariate and Lasso-Cox regression, with nomogram construction and survival analysis. Single-cell RNA sequencing data (GSE223373) were further analyzed to characterize cellular heterogeneity and the cell-type-specific expression patterns of the identified key genes.ResultsSeventy-nine candidate genes associated with Wilms tumor were identified using multidimensional intersection analysis. These genes were significantly involved in pathways such as microRNAs in cancer and the cell cycle. Univariate Cox and Lasso-Cox regression analyses identified and as key genes closely associated with the prognosis of patients with Wilms tumor. Kaplan-Meier survival analysis demonstrated that higher expressions of and were significantly associated with better overall survival in these patients. The nomogram model constructed based on the two key genes demonstrated excellent calibration (area under the curve > 0.8) and clinical applicability. Network analysis identified , the hsa-let-7 microRNA, and transcription factors such as and were as core regulatory nodes. Single-cell analysis demonstrated pronounced stromal expansion within Wilms tumor specimens and further revealed that was preferentially enriched in tumor epithelial cells, whereas exhibited a stromal-skewed distribution, predominantly within mesangial cells.Conclusions and were identified as key prognostic genes for Wilms tumor. These findings suggest that formaldehyde exposure is associated with Wilms tumor pathogenesis through the potential involvement of cancer-associated microRNA pathways and cell cycle signaling, which could contribute to dysregulated cell proliferation and apoptosis. - Source: PubMed
Publication date: 2026/09/22
Li Gui JunZhang ShengChang Li NaLi Zhong XianDuan Yang YangLiu Qi - Cancer stem cells (CSCs) are a therapy-refractory subpopulation that drives tumor persistence, recurrence, and metastasis. A defining characteristic of CSCs is their ability to reversibly exit the cell cycle and enter a quiescent state, thereby escaping cytotoxic therapies that primarily target proliferating cells. Although numerous reviews have examined CSC dormancy and quiescence, less attention has been devoted to recently identified regulators and to the molecular events associated with the transition into quiescence. This narrative review consolidates current knowledge on CSC-specific entry regulators, including the pRb/RBL2-E2F1/4-GCN5 axis, Fbxw7-c-Myc pathway, PML-PPARδ-FAO axis, ID1/ID3-p21 network, JARID1B-mediated G-like states, CDH1-SIRT5-Cyclin F axis, and AP-1/ETS network, alongside emerging evidence on epigenetic regulation, circadian influences, and immune-mediated signals. We critically evaluate the exhaustion hypothesis, delineate a therapeutic framework that distinguishes between prevention of quiescence entry, elimination of dormant CSCs, and forced reactivation, and identify key knowledge gaps. By integrating recent advances within a structured perspective, this review provides a framework for understanding how CSCs exploit quiescence for survival and therapy resistance and informs strategies to target this resilient population. - Source: PubMed
Ahmadi YasinAbdullah Trefa MAbolhasani SakhavatJalizi Amin - - Source: PubMed
Publication date: 2026/09/21
Cui HuanhuanLiang WeizhengShi ZhaoyingZhang LumingLi GuipengChen RuiTian ChiGan DiwenShi XinyaoSun ZhiyuanZhu QionghuaFang LiangHuang HongdaHu YuhuiChen YonglongChen Wei - Diffuse large B-cell lymphoma (DLBCL) is a highly heterogeneous malignancy in which metabolic adaptation contributes to aggressive behavior and treatment resistance. Although TRIM28 has been implicated in several cancers, its role in DLBCL remains unclear. Here, we investigated the function of TRIM28 in DLBCL progression and glycolytic reprogramming. TRIM28 expression was elevated in the TCGA DLBC cohort and in DLBCL cell lines compared with the normal B-cell line GM12878, and it was positively correlated with PKM2 expression in GEPIA. Gain- and loss-of-function assays showed that TRIM28 promoted cell proliferation and migration while suppressing apoptosis. Metabolic analyses further demonstrated that TRIM28 increased extracellular acidification, ATP production, lactate generation, and the expression of glycolysis-related genes, including PFKFB3, HK2, and PKM2. Mechanistically, bioinformatic analysis and dual-luciferase reporter assays identified PKM2 as a transcriptional target of E2F1, and TRIM28 upregulated E2F1 at both mRNA and protein levels, suggesting that TRIM28 acts upstream of the E2F1/PKM2 axis. Importantly, silencing either E2F1 or PKM2 markedly attenuated the effects of TRIM28 on DLBCL cell growth, migration, and glycolytic activity. In a xenograft model, TRIM28 overexpression accelerated tumor growth, whereas E2F1 or PKM2 knockdown significantly reversed these effects. Collectively, TRIM28 facilitates DLBCL progression by inducing glycolytic reprogramming through the E2F1/PKM2 axis, highlighting a potential therapeutic target. - Source: PubMed
Publication date: 2026/09/19
Xin LiuyanLi AnXiao WeiYu JiaqiWang Feilin - The escalating incidence and mortality rates of hepatocellular carcinoma (HCC), coupled with delayed diagnosis, resistance to existing therapies, and profound molecular heterogeneity, underscore the urgent need for improved, clinically actionable biomarkers. - Source: PubMed
Publication date: 2026/09/15
Jain RashiPuri VeenaMungamuri Sathish KumarGarg Prabha