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Published on: May 14, 2016
Nuclear translocation during the cross-talk between cellular stress, cell cycle and anticancer agents
1Department of Experimental Pharmacology, Medical School, University of Athens, M. Asias 75, GR-11527 Athens, Greece. aityliga@med.uoa.gr
Abstract:
The function of many endogenous molecules in all eukaryotic cells depends on their subcellular localisation, being active when localized in one cellular compartment and inactive in another. Translocation or re-localization of mislocalized components in the optimal subcellular site may contribute to the development of novel cancer therapies and to the re-evaluation of conventional treatment. For instance, various agents are able to entrap cytoplasmic anti-apoptotic pathways to the nucleus, thus activating apoptosis. Moreover, amongst the factors identified so far, the optimal location of the tumor suppressor p53 for promoting cell arrest and apoptosis seems to be the nucleus, while the nuclear factor kappa B (NFkappaB) is desirable to stay in the cytoplasm. Thus, the mechanisms of nuclear translocation of endogenous signaling components, like p53, NFkappaB and various heat shock proteins (HSPs), may serve as targets for pharmacological intervention, without excluding the possible role of uptake and active transport into the nucleus of extracellular proteins.
Insights
Subcellular localization of molecules is crucial for cell function. Targeting the movement of these molecules, like p53 and NF-kappaB, to optimal cellular sites offers novel cancer therapy strategies.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- The function of endogenous molecules in eukaryotic cells is dependent on their subcellular localization.
- Mislocalized molecules can impact cellular processes, offering potential therapeutic targets.
Purpose of the Study:
- To explore the role of subcellular translocation of molecules in cellular function and cancer.
- To identify mechanisms of nuclear translocation as potential targets for pharmacological intervention.
Main Methods:
- Review of existing literature on molecular translocation and its role in apoptosis and cell cycle arrest.
- Analysis of the subcellular localization of key signaling molecules such as p53, NF-kappaB, and heat shock proteins (HSPs).
Main Results:
- Optimal localization of tumor suppressor p53 in the nucleus promotes cell arrest and apoptosis.
- Keeping nuclear factor kappa B (NFkappaB) in the cytoplasm is desirable for cellular regulation.
- Mechanisms governing the nuclear translocation of p53, NFkappaB, and HSPs can be targeted for therapeutic strategies.
Conclusions:
- Re-localizing mislocalized cellular components to their optimal sites can lead to novel cancer therapies.
- Targeting the nuclear translocation mechanisms of signaling molecules presents a promising avenue for cancer treatment.
- The uptake and transport of extracellular proteins into the nucleus may also play a role in therapeutic interventions.
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