| ERK activation by thymosin-beta-4 (TB4) overexpression induces paclitaxel-resistance. | |
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MedLine Citation:
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PMID: 16515784 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The development of paclitaxel-resistance in tumors is one of the most significant obstacles to successful therapy. Thymosin-beta-4 (TB4) has been known as actin-sequestering protein and functions in tumor metastasis. Here, we overexpressed TB4 in HeLa cells (TB4-HeLa) and examined the effect of TB4 in paclitaxel-induced cell death. TB4-HeLa cells showed a higher growth rate and a lower percentage of basal apoptosis than HeLa cells. TB4-HeLa cells were more resistant to paclitaxel-induced cell death than HeLa cells. TB4 transcript expression with paclitaxel treatment was dose-dependently increased in HeLa cells but that was not in TB4-HeLa cells. Small interfering RNA (siRNA) of TB4 inhibited HeLa cell growth and enhanced paclitaxel-induced cell death. Basal ERK phosphorylation was elevated and basal p38 kinase phosphorylation was reduced in paclitaxel non-treated TB4-HeLa cells. When treated with paclitaxel, cell death and resistance-induction were independent of ERK and p38 kinase activation. Paclitaxel-resistance of TB4-HeLa cells was overcome by the inhibition of basal ERK activity with PD98059 pre-treatment. The inhibition of basal p38 kinase activity with SB203580 pre-treatment attenuated the paclitaxel-induced HeLa cell death. In conclusion, TB4 induced paclitaxel-resistance through the elevation of basal level of ERK phosphorylation. Therefore, TB4 could be a novel target to regulate paclitaxel-resistance. |
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Authors:
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Su-Young Oh; Ji-Hee Song; Jung-Eun Gil; Jeong-Hee Kim; Young-Il Yeom; Eun-Yi Moon |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2006-03-03 |
Journal Detail:
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Title: Experimental cell research Volume: 312 ISSN: 0014-4827 ISO Abbreviation: Exp. Cell Res. Publication Date: 2006 May |
Date Detail:
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Created Date: 2006-05-02 Completed Date: 2006-07-21 Revised Date: 2013-06-03 |
Medline Journal Info:
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Nlm Unique ID: 0373226 Medline TA: Exp Cell Res Country: United States |
Other Details:
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Languages: eng Pagination: 1651-7 Citation Subset: IM |
Affiliation:
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Department of Human Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Taejeon 305-806, Korea. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antineoplastic Agents, Phytogenic / pharmacology Apoptosis / drug effects, genetics Cell Proliferation Cell Survival / drug effects, genetics Drug Resistance, Neoplasm / genetics* Enzyme Activation Enzyme Inhibitors / pharmacology Extracellular Signal-Regulated MAP Kinases / metabolism* Flavonoids / pharmacology Gene Expression Regulation, Neoplastic HeLa Cells Humans Imidazoles / pharmacology Mice NIH 3T3 Cells Paclitaxel / pharmacology* Phosphorylation / drug effects Pyridines / pharmacology RNA, Small Interfering / genetics Thymosin / genetics*, metabolism Transfection p38 Mitogen-Activated Protein Kinases / metabolism ras Proteins / genetics |
| Chemical | |
Reg. No./Substance:
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0/2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0/Antineoplastic Agents, Phytogenic; 0/Enzyme Inhibitors; 0/Flavonoids; 0/Imidazoles; 0/Pyridines; 0/RNA, Small Interfering; 0/SB 203580; 33069-62-4/Paclitaxel; 61512-21-8/Thymosin; 77591-33-4/thymosin beta(4); EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases; EC 3.6.5.2/ras Proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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