ArticleCell cycle (Georgetown, Tex.)2017
Inhibition of E2F1 activity and cell cycle progression by arsenic via retinoblastoma protein.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 63 citations in OpenAlex.
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- Arsenic impairs Drosophila neural stem cell mitotic progression and sleep behavior in a tauopathy model.G3 (Bethesda, Md.) · 2025Article
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- DTL promotes the growth and migration of melanoma cells through the ERK/E2F1/BUB1 axis.Scientific reports · 2024Article
- Unveiling the link between arsenic toxicity and diabetes: an in silico exploration into the role of transcription factors.Toxicological research · 2024Article
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- Novel strategy for activating gene expression through triplex DNA formation targeting epigenetically suppressed genes.RSC chemical biology · 2024Article
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- Single-cell sequencing revealed metabolic reprogramming and its transcription factor regulatory network in prostate cancer.Translational oncology · 2024Article
- Anti-Müllerian hormone: biology and role in endocrinology and cancers.Frontiers in endocrinology · 2024Review
- N-linked glycosylation is essential for anti-tumor activities of KIAA1324 in gastric cancer.Cell death & disease · 2023Article
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- Upregulation of miR-20a-5p as the Potential MicroRNA Marker in Red Blood Cell Storage Lesion.BioMed research international · 2023Article
- Aspirin Mediates Its Antitumoral Effect Through Inhibiting PTTG1 in Pituitary Adenoma.The Journal of clinical endocrinology and metabolism · 2022Article
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- Unique Transcriptomic Changes Underlie Hormonal Interactions During Mammary Histomorphogenesis in Female Pigs.Endocrinology · 2022Article
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1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The regulation of cell cycle progression by steroid hormones and growth factors is important for maintaining normal cellular processes including development and cell proliferation. Deregulated progression through the G1/S and G2/M cell cycle transitions can lead to uncontrolled cell proliferation and cancer. The transcription factor E2F1, a key cell cycle regulator, targets genes encoding proteins that regulate cell cycle progression through the G1/S transition as well as proteins important in DNA repair and apoptosis. E2F1 expression and activity is inhibited by inorganic arsenic (iAs) that has a dual role as a cancer therapeutic and as a toxin that leads to diseases including cancer. An understanding of what underlies this dichotomy will contribute to understanding how to use iAs as a more effective therapeutic and also how to treat cancers that iAs promotes. Here, we show that quiescent breast adenocarcinoma MCF-7 cells treated with 17-β estradiol (E2) progress through the cell cycle, but few cells treated with E2 + iAs progress from G1 into S-phase due to a block in cell cycle progression. Our data support a model in which iAs inhibits the dissociation of E2F1 from the tumor suppressor, retinoblastoma protein (pRB) due to changes in pRB phosphorylation which leads to decreased E2F1 transcriptional activity. These findings present an explanation for how iAs can disrupt cell cycle progression through E2F1-pRB and has implications for how iAs acts as a cancer therapeutic as well as how it may promote tumorigenesis through decreased DNA repair.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.