ArticleInvestigational new drugs2001
Mechanisms of action of the novel sulfonamide anticancer agent E7070 on cell cycle progression in human non-small cell lung cancer cells.
Article in Investigational new drugs, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 113 citations in OpenAlex.
- Trial
- Human metabolism of [(14)C]indisulam following i.v. infusion in cancer patients.Investigational new drugs · 2005Trial
- Inhibition of RNA splicing is a novel therapeutic strategy for disruption of nuclear replicating viruses.bioRxiv : the preprint server for biology · 2026Article
- Methylation of RBM39 by PRMT6 enhances resistance to Indisulam in non-small cell lung cancer by promoting alternative splicing of proto-oncogenes.PLoS biology · 2025Article
- Identification of E3 Ubiquitin Ligase Substrates Using Biotin Ligase-Based Proximity Labeling Approaches.Biomedicines · 2025Review
- Article
- Recent advances in anticancer mechanisms of molecular glue degraders: focus on RBM39-dgrading synthetic sulfonamide such as indisulam, E7820, tasisulam, and chloroquinoxaline sulfonamide.Genes & genomics · 2024Review
- Novel sulfonamides unveiled as potent anti-lung cancer agentsRSC medicinal chemistry · 2024Article
- Applications of protein ubiquitylation and deubiquitylation in drug discovery.The Journal of biological chemistry · 2024Review
- Indisulam synergizes with melphalan to inhibit Multiple Myeloma malignancy via targeting TOP2A.PloS one · 2024Article
- Inflammation as a driver of hematological malignancies.Frontiers in oncology · 2024Review
- Theoretical Study on the Alkylimino-Substituted Sulfonamides with Potential Biological Activity.The journal of physical chemistry. B · 2023Article
- Overlaid Transcriptional and Proteome Analyses Identify Mitotic Kinesins as Important Targets of Arylsulfonamide-Mediated RBM39 Degradation.Molecular cancer research : MCR · 2023Article
- Therapeutic Targeting of RNA Splicing in Cancer.Genes · 2023Review
- Indisulam exerts anticancer effects via modulation of transcription, translation and alternative splicing on human cervical cancer cells.American journal of cancer research · 2023Article
- Indisulam Reduces Viability and Regulates Apoptotic Gene Expression in Pediatric High-Grade Glioma Cells.Biomedicines · 2022Article
- Genetic and compound screens uncover factors modulating cancer cell response to indisulam.Life science alliance · 2022Article
- PROTAC targeted protein degraders: the past is prologue.Nature reviews. Drug discovery · 2022Review
- Indisulam synergizes with palbociclib to induce senescence through inhibition of CDK2 kinase activity.PloS one · 2022Article
- The Carbonic Anhydrase Inhibitor E7070 Sensitizes Glioblastoma Cells to Radio- and Chemotherapy and Reduces Tumor Growth.Molecular neurobiology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E7070 is a novel sulfonamide antitumor agent that exhibits potent antitumor activity in vitro and in vivo. This compound affects cell cycle progression in human tumor cells. To elucidate the mechanisms by which E7070 inhibits tumor cell growth, we established and characterized an E7070-resistant subline, A549/ER, from a human non-small cell lung cancer cell line A549. Flow cytometric analyses demonstrated an increase in G0/G1 and a decrease in S phase populations in cells treated with E7070 at 20 or 100 microg/ml for 24 h. Longer exposure to E7070, i.e. 48 and 72 h, increased the G2/M phase fraction in A549 cells. These inhibitory actions of E7070 on cell cycle progression were not observed in A549/ER cells. E7070 inhibited the phosphorylation of pRb, decreased expressions of cyclin A, B1, CDK2, and CDC2 proteins, and suppressed CDK2 catalytic activity with the induction of p53 and p21 proteins in A549 cells but not in A549/ER cells. Taken together, these results suggest that E7070 exerts its antitumor effects by disturbing the cell cycle at multiple points, including both the G1/S and the G2/M transition, in human lung cancer cells.
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