Effect of selective cyclooxygenase 2 inhibitor in TCDD pre-exposed thyroid papillary carcinoma cell line

Hae Sung Kim, Kwang Sung Ahn, Jeong Hyeon Lee, Yang Seok Chae, Nam Hee Won, Jong Sang Choi, Chul Hwan Kim

Research output: Contribution to journalArticle

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Abstract

Background: Cyclooxygenase 2 (COX-2) is related to carcinogenesis and progression of cancer. COX-2 has been detected in thyroid cancer. This suggests that COX-2 inhibitor may be useful to control the growth of thyroid cancer cells as well as the progression of thyroid cancer. Tetrachlo-rodibenzodioxin (TCDD), acting as an infammatory cytokine, directly induces the expression of COX-2. We examine whether TCDD controls the effect of COX-2 inhibitor on thyroid cancer cells. Methods: The effects of TCDD and celecoxib on thyroid papillary carcinoma cell line (SNU790) were examined using cell proliferation and fluorescence-activated cell sorting analysis. Western blot analysis was performed to determine the expressed COX-2 levels and the cell cycle-related proteins. The matrix metalloproteinase-2 (MMP-2) expression and gelatinolytic activity were examined using real time-polymerase chain reaction and zymography. Results: TCDD directly induced the growth of SNU790 and the expression of cyclin D1, cyclin A, cyclin E, p21 and COX-2. Celecoxib suppressed the growth of SNU790 and the expression of cyclin D1 and cyclin E. Celecoxib reduced the MMP-2 expression and the gelatinolytic activity, but those effects were decreased in the SNU790 by either pre-treatment with TCDD or co-treatment with TCDD and celecoxib. Conclusions: Celocoxib effect is directly reduced depending on the exposure to TCDD. TCDD exposure should be considered in the treatment with Celecoxib.

Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalKorean Journal of Pathology
Volume45
Issue number1
DOIs
Publication statusPublished - 2011 Feb 1

Fingerprint

Celecoxib
Cyclooxygenase 2 Inhibitors
Cyclooxygenase 2
Thyroid Neoplasms
Cell Line
Cyclin E
Matrix Metalloproteinase 2
Cyclin D1
Growth
Cyclin A
Cell Cycle Proteins
Real-Time Polymerase Chain Reaction
Flow Cytometry
Carcinogenesis
Western Blotting
Cell Proliferation
Papillary Thyroid cancer
Cytokines

Keywords

  • Carcinoma, papillary
  • Cyclooxygenase 2
  • Cyclooxygenase 2 inhibitors
  • Tetrachlorodibenzodioxin
  • Thyroid gland

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Effect of selective cyclooxygenase 2 inhibitor in TCDD pre-exposed thyroid papillary carcinoma cell line. / Kim, Hae Sung; Ahn, Kwang Sung; Lee, Jeong Hyeon; Chae, Yang Seok; Won, Nam Hee; Choi, Jong Sang; Kim, Chul Hwan.

In: Korean Journal of Pathology, Vol. 45, No. 1, 01.02.2011, p. 1-8.

Research output: Contribution to journalArticle

Kim, Hae Sung ; Ahn, Kwang Sung ; Lee, Jeong Hyeon ; Chae, Yang Seok ; Won, Nam Hee ; Choi, Jong Sang ; Kim, Chul Hwan. / Effect of selective cyclooxygenase 2 inhibitor in TCDD pre-exposed thyroid papillary carcinoma cell line. In: Korean Journal of Pathology. 2011 ; Vol. 45, No. 1. pp. 1-8.
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AU - Kim, Chul Hwan

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N2 - Background: Cyclooxygenase 2 (COX-2) is related to carcinogenesis and progression of cancer. COX-2 has been detected in thyroid cancer. This suggests that COX-2 inhibitor may be useful to control the growth of thyroid cancer cells as well as the progression of thyroid cancer. Tetrachlo-rodibenzodioxin (TCDD), acting as an infammatory cytokine, directly induces the expression of COX-2. We examine whether TCDD controls the effect of COX-2 inhibitor on thyroid cancer cells. Methods: The effects of TCDD and celecoxib on thyroid papillary carcinoma cell line (SNU790) were examined using cell proliferation and fluorescence-activated cell sorting analysis. Western blot analysis was performed to determine the expressed COX-2 levels and the cell cycle-related proteins. The matrix metalloproteinase-2 (MMP-2) expression and gelatinolytic activity were examined using real time-polymerase chain reaction and zymography. Results: TCDD directly induced the growth of SNU790 and the expression of cyclin D1, cyclin A, cyclin E, p21 and COX-2. Celecoxib suppressed the growth of SNU790 and the expression of cyclin D1 and cyclin E. Celecoxib reduced the MMP-2 expression and the gelatinolytic activity, but those effects were decreased in the SNU790 by either pre-treatment with TCDD or co-treatment with TCDD and celecoxib. Conclusions: Celocoxib effect is directly reduced depending on the exposure to TCDD. TCDD exposure should be considered in the treatment with Celecoxib.

AB - Background: Cyclooxygenase 2 (COX-2) is related to carcinogenesis and progression of cancer. COX-2 has been detected in thyroid cancer. This suggests that COX-2 inhibitor may be useful to control the growth of thyroid cancer cells as well as the progression of thyroid cancer. Tetrachlo-rodibenzodioxin (TCDD), acting as an infammatory cytokine, directly induces the expression of COX-2. We examine whether TCDD controls the effect of COX-2 inhibitor on thyroid cancer cells. Methods: The effects of TCDD and celecoxib on thyroid papillary carcinoma cell line (SNU790) were examined using cell proliferation and fluorescence-activated cell sorting analysis. Western blot analysis was performed to determine the expressed COX-2 levels and the cell cycle-related proteins. The matrix metalloproteinase-2 (MMP-2) expression and gelatinolytic activity were examined using real time-polymerase chain reaction and zymography. Results: TCDD directly induced the growth of SNU790 and the expression of cyclin D1, cyclin A, cyclin E, p21 and COX-2. Celecoxib suppressed the growth of SNU790 and the expression of cyclin D1 and cyclin E. Celecoxib reduced the MMP-2 expression and the gelatinolytic activity, but those effects were decreased in the SNU790 by either pre-treatment with TCDD or co-treatment with TCDD and celecoxib. Conclusions: Celocoxib effect is directly reduced depending on the exposure to TCDD. TCDD exposure should be considered in the treatment with Celecoxib.

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