Troglitazone activates p21Cip/WAF1 through the ERK pathway in HCT15 human colorectal cancer cells

Jin Ah Kim; Ki Sook Park; Ha Il Kim; So Young Oh; Yongho Ahn; Jong Won Oh; Kang Yell Choi

doi:10.1016/S0304-3835(01)00869-2

Troglitazone activates p21^Cip/WAF1 through the ERK pathway in HCT15 human colorectal cancer cells

Jin Ah Kim, Ki Sook Park, Ha Il Kim, So Young Oh, Yongho Ahn, Jong Won Oh, Kang Yell Choi

Research output: Contribution to journal › Article › peer-review

29 Citations (Scopus)

Abstract

In this study, we identified a new mechanism for the anti-proliferation of HCT15 colorectal cancer cells by troglitazone (TRO). Treating HCT15 cells with 20μM of TRO transiently increased extracellular signal regulated kinase (ERK) activity within 15min, and this subsequently induced p21^Cip/WAF1 cell cycle regulator and localized in the nucleus. Raf-1 modification and MEK activation also occurred after TRO treatment, and Elk-1-dependent trans-reporter gene expression was concomitantly induced. The induction and nuclear localization of p21^Cip/WAF1 by TRO were blocked by PD98059 pre-treatment, which suggested a role for the ERK pathway in p21^Cip/WAF1 activation. TRO inhibited BrdU incorporation and no BrdU incorporation was observed in most p21^Cip/WAF1-activated cells. Therefore, TRO regulates the proliferation of HCT15 cells at least partly by a mechanism involving the activation of p21^Cip/WAF1.

Original language	English
Pages (from-to)	185-195
Number of pages	11
Journal	Cancer Letters
Volume	179
Issue number	2
DOIs	https://doi.org/10.1016/S0304-3835(01)00869-2
Publication status	Published - 2002 May 28

Bibliographical note

Funding Information:
We would like to thank Drs G. Johnson and J.H. Kim for providing kinase inactive MEK and dominant inhibitory Raf-1 kinase construct, respectively. This work was supported by the following grants to K.-Y.C.: the 1999 Korean National Cancer Control Program, Ministry of Health and Welfare, Korea; grant 1999-1-212-001-5 from the basic research program, and Research Center for Biomedical Resources of the Korean Science and Engineering Foundation. J.-A.K., K.-S.P. and H.-I.K. are recipients of a scholarship from the Brain Korea 21 Project for Medical Science, Ministry of Education, Korea.

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S0304-3835(01)00869-2

Cite this

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title = "Troglitazone activates p21Cip/WAF1 through the ERK pathway in HCT15 human colorectal cancer cells",

abstract = "In this study, we identified a new mechanism for the anti-proliferation of HCT15 colorectal cancer cells by troglitazone (TRO). Treating HCT15 cells with 20μM of TRO transiently increased extracellular signal regulated kinase (ERK) activity within 15min, and this subsequently induced p21Cip/WAF1 cell cycle regulator and localized in the nucleus. Raf-1 modification and MEK activation also occurred after TRO treatment, and Elk-1-dependent trans-reporter gene expression was concomitantly induced. The induction and nuclear localization of p21Cip/WAF1 by TRO were blocked by PD98059 pre-treatment, which suggested a role for the ERK pathway in p21Cip/WAF1 activation. TRO inhibited BrdU incorporation and no BrdU incorporation was observed in most p21Cip/WAF1-activated cells. Therefore, TRO regulates the proliferation of HCT15 cells at least partly by a mechanism involving the activation of p21Cip/WAF1.",

author = "Kim, {Jin Ah} and Park, {Ki Sook} and Kim, {Ha Il} and Oh, {So Young} and Yongho Ahn and Oh, {Jong Won} and Choi, {Kang Yell}",

note = "Funding Information: We would like to thank Drs G. Johnson and J.H. Kim for providing kinase inactive MEK and dominant inhibitory Raf-1 kinase construct, respectively. This work was supported by the following grants to K.-Y.C.: the 1999 Korean National Cancer Control Program, Ministry of Health and Welfare, Korea; grant 1999-1-212-001-5 from the basic research program, and Research Center for Biomedical Resources of the Korean Science and Engineering Foundation. J.-A.K., K.-S.P. and H.-I.K. are recipients of a scholarship from the Brain Korea 21 Project for Medical Science, Ministry of Education, Korea.",

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AU - Kim, Jin Ah

AU - Park, Ki Sook

AU - Kim, Ha Il

AU - Oh, So Young

AU - Ahn, Yongho

AU - Oh, Jong Won

AU - Choi, Kang Yell

N1 - Funding Information: We would like to thank Drs G. Johnson and J.H. Kim for providing kinase inactive MEK and dominant inhibitory Raf-1 kinase construct, respectively. This work was supported by the following grants to K.-Y.C.: the 1999 Korean National Cancer Control Program, Ministry of Health and Welfare, Korea; grant 1999-1-212-001-5 from the basic research program, and Research Center for Biomedical Resources of the Korean Science and Engineering Foundation. J.-A.K., K.-S.P. and H.-I.K. are recipients of a scholarship from the Brain Korea 21 Project for Medical Science, Ministry of Education, Korea.

PY - 2002/5/28

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N2 - In this study, we identified a new mechanism for the anti-proliferation of HCT15 colorectal cancer cells by troglitazone (TRO). Treating HCT15 cells with 20μM of TRO transiently increased extracellular signal regulated kinase (ERK) activity within 15min, and this subsequently induced p21Cip/WAF1 cell cycle regulator and localized in the nucleus. Raf-1 modification and MEK activation also occurred after TRO treatment, and Elk-1-dependent trans-reporter gene expression was concomitantly induced. The induction and nuclear localization of p21Cip/WAF1 by TRO were blocked by PD98059 pre-treatment, which suggested a role for the ERK pathway in p21Cip/WAF1 activation. TRO inhibited BrdU incorporation and no BrdU incorporation was observed in most p21Cip/WAF1-activated cells. Therefore, TRO regulates the proliferation of HCT15 cells at least partly by a mechanism involving the activation of p21Cip/WAF1.

AB - In this study, we identified a new mechanism for the anti-proliferation of HCT15 colorectal cancer cells by troglitazone (TRO). Treating HCT15 cells with 20μM of TRO transiently increased extracellular signal regulated kinase (ERK) activity within 15min, and this subsequently induced p21Cip/WAF1 cell cycle regulator and localized in the nucleus. Raf-1 modification and MEK activation also occurred after TRO treatment, and Elk-1-dependent trans-reporter gene expression was concomitantly induced. The induction and nuclear localization of p21Cip/WAF1 by TRO were blocked by PD98059 pre-treatment, which suggested a role for the ERK pathway in p21Cip/WAF1 activation. TRO inhibited BrdU incorporation and no BrdU incorporation was observed in most p21Cip/WAF1-activated cells. Therefore, TRO regulates the proliferation of HCT15 cells at least partly by a mechanism involving the activation of p21Cip/WAF1.

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