Artemin reduces sensitivity to doxorubicin and paclitaxel in endometrial carcinoma cells through specific regulation of CD24

Pandey, Vijay, Jung, Yewon, Kang, Jian, Steiner, Michael, Qian, Peng-Xu, Banerjee, Arindam, Mitchell, Murray D., Wu, Zheng-Sheng, Zhu, T., Liu, Dong-Xu and Lobie, Peter E. (2010) Artemin reduces sensitivity to doxorubicin and paclitaxel in endometrial carcinoma cells through specific regulation of CD24. Translational Oncology, 3 4: 218-229. doi:10.1593/tlo.09325

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Author Pandey, Vijay
Jung, Yewon
Kang, Jian
Steiner, Michael
Qian, Peng-Xu
Banerjee, Arindam
Mitchell, Murray D.
Wu, Zheng-Sheng
Zhu, T.
Liu, Dong-Xu
Lobie, Peter E.
Title Artemin reduces sensitivity to doxorubicin and paclitaxel in endometrial carcinoma cells through specific regulation of CD24
Journal name Translational Oncology   Check publisher's open access policy
ISSN 1936-5233
1944-7124
Publication date 2010-08-01
Year available 2010
Sub-type Article (original research)
DOI 10.1593/tlo.09325
Open Access Status DOI
Volume 3
Issue 4
Start page 218
End page 229
Total pages 12
Place of publication Ann Arbor, MI, United States
Publisher Neoplasia Press
Language eng
Subject 2730 Oncology
1306 Cancer Research
Abstract We have previously reported that artemin (ARTN) stimulates the oncogenicity and invasiveness of endometrial carcinoma cells. Herein, we demonstrate that ARTN modulates the sensitivity of endometrial carcinoma cells to agents used to treat late-stage endometrial carcinoma. Forced expression of ARTN in endometrial carcinoma cells decreased sensitivity to doxorubicin and paclitaxel. Accordingly, depletion of ARTN by small interfering RNA or functional inhibition of ARTN with antibodies significantly increased sensitivity of endometrial carcinoma cells to doxorubicin and paclitaxel. Forced expression of ARTN in endometrial carcinoma cells abrogated doxorubicin-induced G(2)-M arrest and paclitaxel-induced apoptosis. ARTN increased CD24 expression in endometrial carcinoma cells by transcriptional up-regulation, and CD24 was partially correlated to ARTN expression in endometrial carcinoma. Forced expression of CD24 in endometrial carcinoma cells stimulated cell proliferation and oncogenicity, enhanced cell invasion, and decreased sensitivity to doxorubicin and paclitaxel. Depletion of CD24 in endometrial carcinoma cells abrogated ARTN-stimulated resistance to doxorubicin and paclitaxel. ARTN-stimulated resistance to doxorubicin and paclitaxel in endometrial carcinoma cells is therefore mediated by the specific regulation of CD24. Functional inhibition of ARTN may therefore be considered as an adjuvant therapeutic approach to improve the response of endometrial carcinoma to specific chemotherapeutic agents.
Formatted abstract
We have previously reported that artemin (ARTN) stimulates the oncogenicity and invasiveness of endometrial carcinoma cells. Herein, we demonstrate that ARTN modulates the sensitivity of endometrial carcinoma cells to agents used to treat late-stage endometrial carcinoma. Forced expression of ARTN in endometrial carcinoma cells decreased sensitivity to doxorubicin and paclitaxel. Accordingly, depletion of ARTN by small interfering RNA or functional inhibition of ARTN with antibodies significantly increased sensitivity of endometrial carcinoma cells to doxorubicin and paclitaxel. Forced expression of ARTN in endometrial carcinoma cells abrogated doxorubicininduced G2-M arrest and paclitaxel-induced apoptosis. ARTN increased CD24 expression in endometrial carcinoma cells by transcriptional up-regulation, and CD24 was partially correlated to ARTN expression in endometrial carcinoma. Forced expression of CD24 in endometrial carcinoma cells stimulated cell proliferation and oncogenicity, enhanced cell invasion, and decreased sensitivity to doxorubicin and paclitaxel. Depletion of CD24 in endometrial carcinoma cells abrogated ARTN-stimulated resistance to doxorubicin and paclitaxel. ARTN-stimulated resistance to doxorubicin and paclitaxel in endometrial carcinoma cells is therefore mediated by the specific regulation of CD24. Functional inhibition of ARTN may therefore be considered as an adjuvant therapeutic approach to improve the response of endometrial carcinoma to specific chemotherapeutic agents.
© 2010 Neoplasia Press, Inc.
Keyword Independent prognostic marker
Pancreatic-cancer
Breast-cancer
Stimulates oncogenicity
Q-Index Code C1
Q-Index Status Confirmed Code
Grant ID 2007CB914801
30571030
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Faculty of Health and Behavioural Sciences -- Publications
UQ Centre for Clinical Research Publications
Official 2011 Collection
 
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Citation counts: TR Web of Science Citation Count  Cited 19 times in Thomson Reuters Web of Science Article | Citations
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Created: Tue, 22 Feb 2011, 00:16:31 EST by Caroline Irle on behalf of UQ Centre for Clinical Research