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
- Alcohol consumption is associated with increased breast cancer risk, partly due to the accumulation of toxic aldehydes like acetaldehyde, a carcinogenic byproduct of ethanol metabolism. Acetaldehyde Dehydrogenase 2 (ALDH2), a key mitochondrial enzyme, detoxifies acetaldehyde and other reactive aldehydes that drive oxidative stress, DNA damage, and hormonal dysregulation-processes central to carcinogenesis. Although alcohol consumption has been implicated in breast cancer, the role of ALDH2 deficiency itself, in the absence of exogenous alcohol exposure, in mammary gland biology and cancer susceptibility remains unclear. Genetic variants that impair ALDH2 activity are highly prevalent in East Asian populations, where carriers of inactive ALDH2 alleles exhibit impaired aldehyde detoxification. While such individuals are more susceptible to alcohol-related cancers, the effects of ALDH2 deficiency on mammary gland development and homeostasis without alcohol exposure remain unexplored. To investigate the effects of ALDH2 deficiency on mammary proliferation and development, we utilized a C57BL/6-based ALDH2 knockout (Aldh2-/-) mouse model. Our findings revealed that Aldh2-/- mice displayed hyperproliferative mammary glands with increased epithelial cell density, ductal expansion, and increased numbers of Ki67+ cells. Flow cytometry analysis revealed expansion of luminal and basal epithelial subpopulations, accompanied by enhanced mammary epithelial stemness, as indicated by increased mammosphere formation and colony-forming efficiency. At the molecular level, ALDH2 deficiency activated oxidative stress pathways, reflected by elevated 8-OHdG, p38 MAPK, NF-κB, and Nrf2 signaling, along with DNA damage responses involving p53 and H2A.X. We also identified a novel upregulation of RANK and RANKL in Aldh2-/- mammary glands, identifying the RANK/RANKL upregulation associated with NF-κB/p38 MAPK activation and enhanced mammary stemness. Furthermore, hormonal dysregulation was observed, with a significant increase in ERα and PR expression and phosphorylation. Dysregulated ER signaling correlated with enhanced erbB3 activation and downstream signaling, including the cyclin D1-pRb-E2F1 axis. These findings suggest that ALDH2 deficiency, possibly through accumulated endogenous aldehydes, profoundly alters mammary morphogenesis, epithelial repopulation, and stemness. These effects are associated with activation of oxidative stress and DNA damage pathways, together with upregulation of RANKL, estrogen receptor and receptor tyrosine kinase signaling. This study is the first to identify ALDH2 deficiency as a novel factor associated with mammary epithelial alterations that may create a tissue state that could predispose to oncogenic transformation. - Source: PubMed
Publication date: 2026/09/09
Ma ZhikunParris Amanda BLester MilesGissendanner De'jaVasiliou VasilisYang Xiaohe - Gastric ulcer is a common gastrointestinal disorder associated with oxidative stress, inflammation, and disruption of the gastric mucosal barrier. This study investigated the gastroprotective and therapeutic effects of Phoenix dactylifera (Zaghloul) methanolic leaves extract against ethanol-induced gastric ulcer in male Wistar rats. Phenolic quantification of the extract revealed the presence of phenolic (2450.127 mg GAE/g) and flavonoid (2230.00 mg CE/g) contents. LC-ESI-MS-MS analysis led to detection of 23 compounds. Ethanol administration resulted in elevation of MDA, inflammatory modulators (TNF-α, ICAM-1 and IL-10) and reduction of TAC, GSH and cycloxygenase enzymes (COXI and COXII). Expression of E2F1, RAD21, NIBPL, and Vimentin genes was increased via ulcer induction. Treatment with the extract reversed ethanol effects by elevating TAC, GSH, COXI and COXII and reducing MDA, TNF-α, ICAM-1 and IL-10;TNF-α/IL-10 ratio was increased in the ulcerative group and reduced by treatment. Moreover, the extract modulated the expression of E2F1, RAD21, NIBPL, and Vimentin suggesting a potential association with attenuation of epithelial injury and mucosal repair. Histopathological examination demonstrated improvement of the mucosal architecture and mucin production, and reduction of fibrosis. Collectively, these findings demonstrate the impact of ulcer induction and extract treatment on the expression of the studied genes and support the gastroprotective and therapeutic effects of P. dactylifera leaves extract through antioxidant, anti-inflammatory, and mucosal healing activities. Further studies at the protein level using more dosages of the extract are needed to clarify the mechanistic significance of these gene expression changes and the appropriate dose of the extract. - Source: PubMed
Publication date: 2026/09/24
Aly Hanan FMabrouk Mohamed IShalaby Mohamed BHamed Karima AKhalil Wagdy K BSawi Salma ElEl-Feky Amal MElbatanony Marwa MSalim Mohamed SKiwan Hanan S - 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