Abstract
The development of cancer depends on the delicate balance between cell proliferation and programmed cell death. p16INK4a -cyclinD/cdk4-pRb-E2F1 is a critical pathway regulating cell proliferation in which E2F1 is an important downstream effector. Deregulated E2F1 activity due to the aberrance of the upstream components in this pathway, such as inactivation of Rb or p16, or amplification of cyclinD or cdk4, confers growth advantage to cancer cells and has thus become a hallmark of human tumors. In addition to cell proliferation control, compelling evidence indicates that E2F1 can also induce apoptosis under various cellular contexts regardless of p53 status. Given the frequent inactivation of tumor suppressor pRb and p53 in human cancers, E2F1- induced apoptosis might serve as an additional tumor surveillance mechanism to protect the organism from tumor development. E2F1-mediated apoptosis pathway is therefore emerging as a promising target for therapeutic intervention. Here, we review the recent advances in the understanding of E2F1- mediated apoptosis in cancer cells and discuss how these discoveries may expand our view of E2F1 signaling network and contribute to the development of novel therapeutic strategy.
Keywords: E2F1, Apoptosis, cancer, Therapeutic target
Current Molecular Pharmacology
Title: E2F1-Mediated Apoptosis as a Target of Cancer Therapy
Volume: 2
Author(s): Zhenlong Wu and Qiang Yu
Affiliation:
Keywords: E2F1, Apoptosis, cancer, Therapeutic target
Abstract: The development of cancer depends on the delicate balance between cell proliferation and programmed cell death. p16INK4a -cyclinD/cdk4-pRb-E2F1 is a critical pathway regulating cell proliferation in which E2F1 is an important downstream effector. Deregulated E2F1 activity due to the aberrance of the upstream components in this pathway, such as inactivation of Rb or p16, or amplification of cyclinD or cdk4, confers growth advantage to cancer cells and has thus become a hallmark of human tumors. In addition to cell proliferation control, compelling evidence indicates that E2F1 can also induce apoptosis under various cellular contexts regardless of p53 status. Given the frequent inactivation of tumor suppressor pRb and p53 in human cancers, E2F1- induced apoptosis might serve as an additional tumor surveillance mechanism to protect the organism from tumor development. E2F1-mediated apoptosis pathway is therefore emerging as a promising target for therapeutic intervention. Here, we review the recent advances in the understanding of E2F1- mediated apoptosis in cancer cells and discuss how these discoveries may expand our view of E2F1 signaling network and contribute to the development of novel therapeutic strategy.
Export Options
About this article
Cite this article as:
Wu Zhenlong and Yu Qiang, E2F1-Mediated Apoptosis as a Target of Cancer Therapy, Current Molecular Pharmacology 2009; 2 (2) . https://dx.doi.org/10.2174/1874467210902020149
DOI https://dx.doi.org/10.2174/1874467210902020149 |
Print ISSN 1874-4672 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-4702 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
miR-126 as a Therapeutic Agent for Diabetes Mellitus
Current Pharmaceutical Design Inhibition of RET Activated Pathways: Novel Strategies for Therapeutic Intervention in Human Cancers
Current Pharmaceutical Design Role for Poly(ADP-ribose) Polymerase Activation in Diabetic Nephropathy, Neuropathy and Retinopathy
Current Vascular Pharmacology Clinical Trials with Oncolytic Measles Virus: Current Status and Future Prospects
Current Cancer Drug Targets Chromatin Remodeling Agents for Cancer Therapy
Reviews on Recent Clinical Trials High Throughput Screening of Normal and Neoplastic Tissue Samples
Combinatorial Chemistry & High Throughput Screening Newer Avenues for the Treatment of Leptomeningeal Carcinomatosis
Central Nervous System Agents in Medicinal Chemistry An Update on Overcoming MDR1-Mediated Multidrug Resistance in Cancer Chemotherapy
Current Pharmaceutical Design Inhibition of Bacterial Carbonic Anhydrases and Zinc Proteases: From Orphan Targets to Innovative New Antibiotic Drugs
Current Medicinal Chemistry Sera/Organ Lysates of Selected Animals Living in Polluted Environments Exhibit Cytotoxicity against Cancer Cell Lines
Anti-Cancer Agents in Medicinal Chemistry Endometriosis and Gynecological Cancer
Current Women`s Health Reviews Withdrawal Notice: The Recent Advancement in the Field of Super Paramagnetic Iron Oxide Nanoparticles (SPIONs) for Aiming Breast Cancer
Current Drug Metabolism Group-sparse Modeling Drug-kinase Networks for Predicting Combinatorial Drug Sensitivity in Cancer Cells
Current Bioinformatics Carbohydrate Antigens: Synthesis Aspects and Immunological Applications in Cancer
Mini-Reviews in Medicinal Chemistry Near-infrared Light Activatable Multimodal Gold Nanostructures Platform: An Emerging Paradigm for Cancer Therapy
Current Cancer Drug Targets A Novel Lily-of-the-Valley Fragrance Contrast Agent for Magnetic Resonance and Fluorescence Imaging of Prostate Cancer Cells
Current Pharmaceutical Biotechnology Overcoming Resistance of Glioblastoma to Conventional Cytotoxic Therapies by the Addition of PARP Inhibitors
Anti-Cancer Agents in Medicinal Chemistry Inhibiting Cyclin-Dependent Kinase / Cyclin Activity for the Treatment of Cancer and Cardiovascular Disease
Current Pharmaceutical Biotechnology Biomaterial and Stem Cell Interactions: Histological Biocompatibility
Current Stem Cell Research & Therapy Nanostructural Hybrid Sensitizers for Photodynamic Therapy
Current Pharmaceutical Design