ERK activation by Thymosin-beta-4 (TB4) overexpression induces paclitaxel-resistance

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dc.contributor.authorSu-Young Oh-
dc.contributor.authorJun Hee Lee-
dc.contributor.authorJung-Eun Gil-
dc.contributor.authorJ H Kim-
dc.contributor.authorYoung Il Yeom-
dc.contributor.authorEun Yi Moon-
dc.date.accessioned2017-04-19T09:04:23Z-
dc.date.available2017-04-19T09:04:23Z-
dc.date.issued2006-
dc.identifier.issn0014-4827-
dc.identifier.uri10.1016/j.yexcr.2006.01.030ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7387-
dc.description.abstractThe 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.-
dc.publisherElsevier-
dc.titleERK activation by Thymosin-beta-4 (TB4) overexpression induces paclitaxel-resistance-
dc.title.alternativeERK activation by Thymosin-beta-4 (TB4) overexpression induces paclitaxel-resistance-
dc.typeArticle-
dc.citation.titleExperimental Cell Research-
dc.citation.number9-
dc.citation.endPage1657-
dc.citation.startPage1651-
dc.citation.volume312-
dc.contributor.affiliatedAuthorSu-Young Oh-
dc.contributor.affiliatedAuthorJun Hee Lee-
dc.contributor.affiliatedAuthorJung-Eun Gil-
dc.contributor.affiliatedAuthorYoung Il Yeom-
dc.contributor.affiliatedAuthorEun Yi Moon-
dc.contributor.alternativeName오수영-
dc.contributor.alternativeName이준희-
dc.contributor.alternativeName길정은-
dc.contributor.alternativeName김정희-
dc.contributor.alternativeName염영일-
dc.contributor.alternativeName문은이-
dc.identifier.bibliographicCitationExperimental Cell Research, vol. 312, no. 9, pp. 1651-1657-
dc.identifier.doi10.1016/j.yexcr.2006.01.030-
dc.subject.keywordERK-
dc.subject.keywordHeLa cell-
dc.subject.keywordPaclitaxel-
dc.subject.keywordResistance-
dc.subject.keywordThymosin-beta-4-
dc.subject.localERK-
dc.subject.localErk-
dc.subject.localHeLa cell-
dc.subject.localHeLa cells-
dc.subject.localHela cell-
dc.subject.localpaclitaxel-
dc.subject.localPaclitaxel-
dc.subject.localResistance-
dc.subject.localresistance-
dc.subject.localThymosin β4-
dc.subject.localThymosin-beta-4 (TB4)-
dc.subject.localThymosin beta-4-
dc.subject.localThymosin-beta-4-
dc.subject.localthymosin beta-4-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
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