Deoxycholic acid-induced signal transduction in HT-29 cells: role of NF-kappa B and interleukin-8

Dong Ki Lee, Sun Young Park, Soon Koo Baik, Sang Ok Kwon, Jun Mo Chung, Eok Soo Oh, Hyun Soo Kim

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

BACKGROUND/AIMS: Deoxycholic acid (DCA) has been appeared to be an endogenous colon tumor promoter. In this study, we investigated whether DCA induces nuclear factor-kappa B (NF-kappa B) activation and IL-8 expression, and tauroursodeoxycholic acid (TUDC) inhibits this signaling in HT-29 cells. METHODS: After DCA treatments, time courses of NF-kappa B binding activity were determined by electrophoretic mobility shift assay (EMSA). Also, we performed Western blotting of I kappa B alpha to confirm NF-kappa B activation. Time and concentration courses of DCA-induced secretion of IL-8 were measured with ELISA in supernatants of cultured media from the cells. To evaluate the role of NF-kappa B, IL-8 levels were assessed after pretreatment with using phosphorothioate-modified anti-sense oligonucleotides (ODN). Moreover, DCA-induced secretions of IL-8 were measured after pretreatment with TUDC. RESULTS: DCA dose-dependently induced prominent NF-kappa B binding complexes from 30 min to 8 hr and degradation of I kappa B alpha. The secretions of IL-8 were increased with DCA (50-200 micro M) treatment in a time and dose-dependent manner. Pre-incubation of the cells with TUDC (0.1-10 micro M) for 2 hours caused significant decreases in DCA induced IL-8 secretion. However, transient transfection using p50 or p65 AS-ODN showed no effect on IL-8 secretion. CONCLUSIONS: DCA may play as a colonic tumor promoter through anti-apoptotic effect of NF-kappa B activation and IL-8 expression, and DCA-induced NF-kappa B independent IL-8 expression is inhibited by TUDC.

Original languageEnglish
Pages (from-to)176-185
Number of pages10
JournalThe Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
Volume43
Issue number3
Publication statusPublished - 2004 Jan 1

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HT29 Cells
Deoxycholic Acid
NF-kappa B
Interleukin-8
Signal Transduction
I-kappa B Proteins
Carcinogens
Antisense Oligonucleotides
Electrophoretic Mobility Shift Assay
Transfection
Cultured Cells
Colon
Western Blotting
Enzyme-Linked Immunosorbent Assay

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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title = "Deoxycholic acid-induced signal transduction in HT-29 cells: role of NF-kappa B and interleukin-8",
abstract = "BACKGROUND/AIMS: Deoxycholic acid (DCA) has been appeared to be an endogenous colon tumor promoter. In this study, we investigated whether DCA induces nuclear factor-kappa B (NF-kappa B) activation and IL-8 expression, and tauroursodeoxycholic acid (TUDC) inhibits this signaling in HT-29 cells. METHODS: After DCA treatments, time courses of NF-kappa B binding activity were determined by electrophoretic mobility shift assay (EMSA). Also, we performed Western blotting of I kappa B alpha to confirm NF-kappa B activation. Time and concentration courses of DCA-induced secretion of IL-8 were measured with ELISA in supernatants of cultured media from the cells. To evaluate the role of NF-kappa B, IL-8 levels were assessed after pretreatment with using phosphorothioate-modified anti-sense oligonucleotides (ODN). Moreover, DCA-induced secretions of IL-8 were measured after pretreatment with TUDC. RESULTS: DCA dose-dependently induced prominent NF-kappa B binding complexes from 30 min to 8 hr and degradation of I kappa B alpha. The secretions of IL-8 were increased with DCA (50-200 micro M) treatment in a time and dose-dependent manner. Pre-incubation of the cells with TUDC (0.1-10 micro M) for 2 hours caused significant decreases in DCA induced IL-8 secretion. However, transient transfection using p50 or p65 AS-ODN showed no effect on IL-8 secretion. CONCLUSIONS: DCA may play as a colonic tumor promoter through anti-apoptotic effect of NF-kappa B activation and IL-8 expression, and DCA-induced NF-kappa B independent IL-8 expression is inhibited by TUDC.",
author = "Lee, {Dong Ki} and Park, {Sun Young} and Baik, {Soon Koo} and Kwon, {Sang Ok} and Chung, {Jun Mo} and Oh, {Eok Soo} and Kim, {Hyun Soo}",
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Deoxycholic acid-induced signal transduction in HT-29 cells : role of NF-kappa B and interleukin-8. / Lee, Dong Ki; Park, Sun Young; Baik, Soon Koo; Kwon, Sang Ok; Chung, Jun Mo; Oh, Eok Soo; Kim, Hyun Soo.

In: The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi, Vol. 43, No. 3, 01.01.2004, p. 176-185.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Deoxycholic acid-induced signal transduction in HT-29 cells

T2 - role of NF-kappa B and interleukin-8

AU - Lee, Dong Ki

AU - Park, Sun Young

AU - Baik, Soon Koo

AU - Kwon, Sang Ok

AU - Chung, Jun Mo

AU - Oh, Eok Soo

AU - Kim, Hyun Soo

PY - 2004/1/1

Y1 - 2004/1/1

N2 - BACKGROUND/AIMS: Deoxycholic acid (DCA) has been appeared to be an endogenous colon tumor promoter. In this study, we investigated whether DCA induces nuclear factor-kappa B (NF-kappa B) activation and IL-8 expression, and tauroursodeoxycholic acid (TUDC) inhibits this signaling in HT-29 cells. METHODS: After DCA treatments, time courses of NF-kappa B binding activity were determined by electrophoretic mobility shift assay (EMSA). Also, we performed Western blotting of I kappa B alpha to confirm NF-kappa B activation. Time and concentration courses of DCA-induced secretion of IL-8 were measured with ELISA in supernatants of cultured media from the cells. To evaluate the role of NF-kappa B, IL-8 levels were assessed after pretreatment with using phosphorothioate-modified anti-sense oligonucleotides (ODN). Moreover, DCA-induced secretions of IL-8 were measured after pretreatment with TUDC. RESULTS: DCA dose-dependently induced prominent NF-kappa B binding complexes from 30 min to 8 hr and degradation of I kappa B alpha. The secretions of IL-8 were increased with DCA (50-200 micro M) treatment in a time and dose-dependent manner. Pre-incubation of the cells with TUDC (0.1-10 micro M) for 2 hours caused significant decreases in DCA induced IL-8 secretion. However, transient transfection using p50 or p65 AS-ODN showed no effect on IL-8 secretion. CONCLUSIONS: DCA may play as a colonic tumor promoter through anti-apoptotic effect of NF-kappa B activation and IL-8 expression, and DCA-induced NF-kappa B independent IL-8 expression is inhibited by TUDC.

AB - BACKGROUND/AIMS: Deoxycholic acid (DCA) has been appeared to be an endogenous colon tumor promoter. In this study, we investigated whether DCA induces nuclear factor-kappa B (NF-kappa B) activation and IL-8 expression, and tauroursodeoxycholic acid (TUDC) inhibits this signaling in HT-29 cells. METHODS: After DCA treatments, time courses of NF-kappa B binding activity were determined by electrophoretic mobility shift assay (EMSA). Also, we performed Western blotting of I kappa B alpha to confirm NF-kappa B activation. Time and concentration courses of DCA-induced secretion of IL-8 were measured with ELISA in supernatants of cultured media from the cells. To evaluate the role of NF-kappa B, IL-8 levels were assessed after pretreatment with using phosphorothioate-modified anti-sense oligonucleotides (ODN). Moreover, DCA-induced secretions of IL-8 were measured after pretreatment with TUDC. RESULTS: DCA dose-dependently induced prominent NF-kappa B binding complexes from 30 min to 8 hr and degradation of I kappa B alpha. The secretions of IL-8 were increased with DCA (50-200 micro M) treatment in a time and dose-dependent manner. Pre-incubation of the cells with TUDC (0.1-10 micro M) for 2 hours caused significant decreases in DCA induced IL-8 secretion. However, transient transfection using p50 or p65 AS-ODN showed no effect on IL-8 secretion. CONCLUSIONS: DCA may play as a colonic tumor promoter through anti-apoptotic effect of NF-kappa B activation and IL-8 expression, and DCA-induced NF-kappa B independent IL-8 expression is inhibited by TUDC.

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