Transcriptional and post-transcriptional regulation of the PKCδ gene by etoposide in L1210 murine leukemia cells: Implication of PKCδ autoregulation

Soon Young Shin; Chang Gun Kim; Jesang Ko; Do Sik Min; Jong Soo Chang; Motoi Ohba; Toshio Kuroki; Young Bong Choi; Young Ho Kim; Doe Sun Na; Jin Woo Kim; Young Han Lee

doi:10.1016/j.jmb.2004.04.006

Transcriptional and post-transcriptional regulation of the PKCδ gene by etoposide in L1210 murine leukemia cells: Implication of PKCδ autoregulation

Soon Young Shin, Chang Gun Kim, Jesang Ko, Do Sik Min, Jong Soo Chang, Motoi Ohba, Toshio Kuroki, Young Bong Choi, Young Ho Kim, Doe Sun Na, Jin Woo Kim, Young Han Lee

Department of Pharmacy

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

16 Citations (Scopus)

Abstract

Protein kinase C δ (PKCδ) plays an important role in the regulation of apoptosis in response to diverse anticancer agents. PKCδ is cleaved irreversibly to a catalytically active fragment in response to apoptotic stimuli; however, little information is available about the regulation of PKCδ gene expression. In this study, we found that the amount of steady-state PKCδ mRNA and protein was increased by etoposide in mouse L1210 leukemia cells. The transcriptional rate of the PKCδ gene and the stability of PKCδ mRNA were increased by treatment with etoposide, resulting in the accumulation of PKCδ protein. Rottlerin inhibited etoposide-induced PKCδ gene expression significantly, while Go6976, LY294002 and PD98059 had no effect. Further, both stable and adenovirus-mediated expression of a dominant negative PKCδ(KR) abrogated etoposide-induced PKCδ expression. Etoposide-stimulated PKCδ transcription but not PKCδ mRNA stability was blocked completely by pretreatment with rottlerin. Our data reveal a novel mechanism whereby PKCδ gene is regulated at the transcriptional and post-transcriptional level in the L1210 leukemia cell line.

Original language	English
Pages (from-to)	681-693
Number of pages	13
Journal	Journal of Molecular Biology
Volume	340
Issue number	4
DOIs	https://doi.org/10.1016/j.jmb.2004.04.006
Publication status	Published - 2004 Jul 16

Bibliographical note

Funding Information:
We thank Dr Sung Ho Ryu (Pohang University of Science and Technology, Korea) for helpful discussion and comments, and Dr Jang-Soo Chun (Kwangju Institute of Science and Technology, Korea) for providing the plasmids pMTH/PKCδ and pMTH/PKCδ(KR). This work was supported by Grant R01-2002-00000167-0 from the Basic Research Program of the Korea Science and Engineering Foundation.

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Molecular Biology

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10.1016/j.jmb.2004.04.006

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Shin, S. Y., Kim, C. G., Ko, J., Min, D. S., Chang, J. S., Ohba, M., Kuroki, T., Choi, Y. B., Kim, Y. H., Na, D. S., Kim, J. W., & Lee, Y. H. (2004). Transcriptional and post-transcriptional regulation of the PKCδ gene by etoposide in L1210 murine leukemia cells: Implication of PKCδ autoregulation. Journal of Molecular Biology, 340(4), 681-693. https://doi.org/10.1016/j.jmb.2004.04.006

@article{4f2055dd0693473382f532798fd669c9,

title = "Transcriptional and post-transcriptional regulation of the PKCδ gene by etoposide in L1210 murine leukemia cells: Implication of PKCδ autoregulation",

abstract = "Protein kinase C δ (PKCδ) plays an important role in the regulation of apoptosis in response to diverse anticancer agents. PKCδ is cleaved irreversibly to a catalytically active fragment in response to apoptotic stimuli; however, little information is available about the regulation of PKCδ gene expression. In this study, we found that the amount of steady-state PKCδ mRNA and protein was increased by etoposide in mouse L1210 leukemia cells. The transcriptional rate of the PKCδ gene and the stability of PKCδ mRNA were increased by treatment with etoposide, resulting in the accumulation of PKCδ protein. Rottlerin inhibited etoposide-induced PKCδ gene expression significantly, while Go6976, LY294002 and PD98059 had no effect. Further, both stable and adenovirus-mediated expression of a dominant negative PKCδ(KR) abrogated etoposide-induced PKCδ expression. Etoposide-stimulated PKCδ transcription but not PKCδ mRNA stability was blocked completely by pretreatment with rottlerin. Our data reveal a novel mechanism whereby PKCδ gene is regulated at the transcriptional and post-transcriptional level in the L1210 leukemia cell line.",

author = "Shin, {Soon Young} and Kim, {Chang Gun} and Jesang Ko and Min, {Do Sik} and Chang, {Jong Soo} and Motoi Ohba and Toshio Kuroki and Choi, {Young Bong} and Kim, {Young Ho} and Na, {Doe Sun} and Kim, {Jin Woo} and Lee, {Young Han}",

note = "Funding Information: We thank Dr Sung Ho Ryu (Pohang University of Science and Technology, Korea) for helpful discussion and comments, and Dr Jang-Soo Chun (Kwangju Institute of Science and Technology, Korea) for providing the plasmids pMTH/PKCδ and pMTH/PKCδ(KR). This work was supported by Grant R01-2002-00000167-0 from the Basic Research Program of the Korea Science and Engineering Foundation.",

year = "2004",

month = jul,

day = "16",

doi = "10.1016/j.jmb.2004.04.006",

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Shin, SY, Kim, CG, Ko, J, Min, DS, Chang, JS, Ohba, M, Kuroki, T, Choi, YB, Kim, YH, Na, DS, Kim, JW & Lee, YH 2004, 'Transcriptional and post-transcriptional regulation of the PKCδ gene by etoposide in L1210 murine leukemia cells: Implication of PKCδ autoregulation', Journal of Molecular Biology, vol. 340, no. 4, pp. 681-693. https://doi.org/10.1016/j.jmb.2004.04.006

TY - JOUR

T1 - Transcriptional and post-transcriptional regulation of the PKCδ gene by etoposide in L1210 murine leukemia cells

T2 - Implication of PKCδ autoregulation

AU - Shin, Soon Young

AU - Kim, Chang Gun

AU - Ko, Jesang

AU - Min, Do Sik

AU - Chang, Jong Soo

AU - Ohba, Motoi

AU - Kuroki, Toshio

AU - Choi, Young Bong

AU - Kim, Young Ho

AU - Na, Doe Sun

AU - Kim, Jin Woo

AU - Lee, Young Han

N1 - Funding Information: We thank Dr Sung Ho Ryu (Pohang University of Science and Technology, Korea) for helpful discussion and comments, and Dr Jang-Soo Chun (Kwangju Institute of Science and Technology, Korea) for providing the plasmids pMTH/PKCδ and pMTH/PKCδ(KR). This work was supported by Grant R01-2002-00000167-0 from the Basic Research Program of the Korea Science and Engineering Foundation.

PY - 2004/7/16

Y1 - 2004/7/16

N2 - Protein kinase C δ (PKCδ) plays an important role in the regulation of apoptosis in response to diverse anticancer agents. PKCδ is cleaved irreversibly to a catalytically active fragment in response to apoptotic stimuli; however, little information is available about the regulation of PKCδ gene expression. In this study, we found that the amount of steady-state PKCδ mRNA and protein was increased by etoposide in mouse L1210 leukemia cells. The transcriptional rate of the PKCδ gene and the stability of PKCδ mRNA were increased by treatment with etoposide, resulting in the accumulation of PKCδ protein. Rottlerin inhibited etoposide-induced PKCδ gene expression significantly, while Go6976, LY294002 and PD98059 had no effect. Further, both stable and adenovirus-mediated expression of a dominant negative PKCδ(KR) abrogated etoposide-induced PKCδ expression. Etoposide-stimulated PKCδ transcription but not PKCδ mRNA stability was blocked completely by pretreatment with rottlerin. Our data reveal a novel mechanism whereby PKCδ gene is regulated at the transcriptional and post-transcriptional level in the L1210 leukemia cell line.

AB - Protein kinase C δ (PKCδ) plays an important role in the regulation of apoptosis in response to diverse anticancer agents. PKCδ is cleaved irreversibly to a catalytically active fragment in response to apoptotic stimuli; however, little information is available about the regulation of PKCδ gene expression. In this study, we found that the amount of steady-state PKCδ mRNA and protein was increased by etoposide in mouse L1210 leukemia cells. The transcriptional rate of the PKCδ gene and the stability of PKCδ mRNA were increased by treatment with etoposide, resulting in the accumulation of PKCδ protein. Rottlerin inhibited etoposide-induced PKCδ gene expression significantly, while Go6976, LY294002 and PD98059 had no effect. Further, both stable and adenovirus-mediated expression of a dominant negative PKCδ(KR) abrogated etoposide-induced PKCδ expression. Etoposide-stimulated PKCδ transcription but not PKCδ mRNA stability was blocked completely by pretreatment with rottlerin. Our data reveal a novel mechanism whereby PKCδ gene is regulated at the transcriptional and post-transcriptional level in the L1210 leukemia cell line.

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U2 - 10.1016/j.jmb.2004.04.006

DO - 10.1016/j.jmb.2004.04.006

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AN - SCOPUS:3042512072

SN - 0022-2836

VL - 340

SP - 681

EP - 693

JO - Journal of Molecular Biology

JF - Journal of Molecular Biology

IS - 4

ER -

Transcriptional and post-transcriptional regulation of the PKCδ gene by etoposide in L1210 murine leukemia cells: Implication of PKCδ autoregulation

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

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