Effects of platelet activating factor, butyrate and interleukin-6 on cyclooxygenase-2 expression in human esophageal cancer cells

Liang Shun Wang, K. C. Chow, Y. C. Wu

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Background: Epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAIDs) can reduce the risk of esophageal squamous cell carcinoma (ESCC) by taking cyclooxygenase (COX) as the target enzyme. The pathophysiological regulation of COX-2 may play a role in carcinogenesis and in disease progression of esophageal carcinoma. Methods: 59 ESCC samples were used to assess COX-2 expression in the tumor cells and four ESCC cell lines to investigate the effects of phorbol myristate acetate (PMA), platelet activating factor (PAF), n-sodium butyrate (n-BT) and interleukin-6 (IL-6) on the expression of COX-2. Expression of COX-2 was determined by immunohistochemistry (IHC) and reverse transcription-polymerase chain reaction (RT-PCR). Production of PGE2 was measured by a competitive enzyme immunoassay (CEIA). Results: COX-2 expression was detected in 54.2% (32/59) of the pathological sections by IHC. COX-2 expression in ESCC cells was significantly increased following treatment with PAF and n-BT. Increased production of PGE2 was detected in the culture media, and the secreted PGE2 in the culture media was proportional to the increased COX-2 expression. The addition of IL-6 could also enhance COX-2 expression in ESCC cells. While NSAIDs could inhibit enzymatic activity of COX-2, they did not inhibit COX-2 gene expression in ESCC cells. PKC inhibitor, however, could abrogate PMA-induced COX-2 gene expression, but it did not block IL-6-induced COX-2 expression. Conclusions: Our data suggest that COX-2 expression in ESCC cells could be upregulated by PMA, PAF, n-BT and IL-6. Nonetheless, IL-6-induced COX-2 expression could be independent of PKC activation.

Original languageEnglish
Pages (from-to)467-475
Number of pages9
JournalScandinavian Journal of Gastroenterology
Volume37
Issue number4
DOIs
Publication statusPublished - 2002
Externally publishedYes

Fingerprint

Butyrates
Platelet Activating Factor
Cyclooxygenase 2
Esophageal Neoplasms
Interleukin-6
Butyric Acid
Tetradecanoylphorbol Acetate
Dinoprostone
Culture Media
Anti-Inflammatory Agents
Immunohistochemistry
Gene Expression
Prostaglandin-Endoperoxide Synthases
Esophageal Squamous Cell Carcinoma
Immunoenzyme Techniques
Pharmaceutical Preparations
Reverse Transcription
Disease Progression
Epidemiologic Studies
Carcinogenesis

Keywords

  • Cyclooxygenase
  • Esophageal carcinoma
  • Inflammation

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Effects of platelet activating factor, butyrate and interleukin-6 on cyclooxygenase-2 expression in human esophageal cancer cells. / Wang, Liang Shun; Chow, K. C.; Wu, Y. C.

In: Scandinavian Journal of Gastroenterology, Vol. 37, No. 4, 2002, p. 467-475.

Research output: Contribution to journalArticle

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abstract = "Background: Epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAIDs) can reduce the risk of esophageal squamous cell carcinoma (ESCC) by taking cyclooxygenase (COX) as the target enzyme. The pathophysiological regulation of COX-2 may play a role in carcinogenesis and in disease progression of esophageal carcinoma. Methods: 59 ESCC samples were used to assess COX-2 expression in the tumor cells and four ESCC cell lines to investigate the effects of phorbol myristate acetate (PMA), platelet activating factor (PAF), n-sodium butyrate (n-BT) and interleukin-6 (IL-6) on the expression of COX-2. Expression of COX-2 was determined by immunohistochemistry (IHC) and reverse transcription-polymerase chain reaction (RT-PCR). Production of PGE2 was measured by a competitive enzyme immunoassay (CEIA). Results: COX-2 expression was detected in 54.2{\%} (32/59) of the pathological sections by IHC. COX-2 expression in ESCC cells was significantly increased following treatment with PAF and n-BT. Increased production of PGE2 was detected in the culture media, and the secreted PGE2 in the culture media was proportional to the increased COX-2 expression. The addition of IL-6 could also enhance COX-2 expression in ESCC cells. While NSAIDs could inhibit enzymatic activity of COX-2, they did not inhibit COX-2 gene expression in ESCC cells. PKC inhibitor, however, could abrogate PMA-induced COX-2 gene expression, but it did not block IL-6-induced COX-2 expression. Conclusions: Our data suggest that COX-2 expression in ESCC cells could be upregulated by PMA, PAF, n-BT and IL-6. Nonetheless, IL-6-induced COX-2 expression could be independent of PKC activation.",
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N2 - Background: Epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAIDs) can reduce the risk of esophageal squamous cell carcinoma (ESCC) by taking cyclooxygenase (COX) as the target enzyme. The pathophysiological regulation of COX-2 may play a role in carcinogenesis and in disease progression of esophageal carcinoma. Methods: 59 ESCC samples were used to assess COX-2 expression in the tumor cells and four ESCC cell lines to investigate the effects of phorbol myristate acetate (PMA), platelet activating factor (PAF), n-sodium butyrate (n-BT) and interleukin-6 (IL-6) on the expression of COX-2. Expression of COX-2 was determined by immunohistochemistry (IHC) and reverse transcription-polymerase chain reaction (RT-PCR). Production of PGE2 was measured by a competitive enzyme immunoassay (CEIA). Results: COX-2 expression was detected in 54.2% (32/59) of the pathological sections by IHC. COX-2 expression in ESCC cells was significantly increased following treatment with PAF and n-BT. Increased production of PGE2 was detected in the culture media, and the secreted PGE2 in the culture media was proportional to the increased COX-2 expression. The addition of IL-6 could also enhance COX-2 expression in ESCC cells. While NSAIDs could inhibit enzymatic activity of COX-2, they did not inhibit COX-2 gene expression in ESCC cells. PKC inhibitor, however, could abrogate PMA-induced COX-2 gene expression, but it did not block IL-6-induced COX-2 expression. Conclusions: Our data suggest that COX-2 expression in ESCC cells could be upregulated by PMA, PAF, n-BT and IL-6. Nonetheless, IL-6-induced COX-2 expression could be independent of PKC activation.

AB - Background: Epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAIDs) can reduce the risk of esophageal squamous cell carcinoma (ESCC) by taking cyclooxygenase (COX) as the target enzyme. The pathophysiological regulation of COX-2 may play a role in carcinogenesis and in disease progression of esophageal carcinoma. Methods: 59 ESCC samples were used to assess COX-2 expression in the tumor cells and four ESCC cell lines to investigate the effects of phorbol myristate acetate (PMA), platelet activating factor (PAF), n-sodium butyrate (n-BT) and interleukin-6 (IL-6) on the expression of COX-2. Expression of COX-2 was determined by immunohistochemistry (IHC) and reverse transcription-polymerase chain reaction (RT-PCR). Production of PGE2 was measured by a competitive enzyme immunoassay (CEIA). Results: COX-2 expression was detected in 54.2% (32/59) of the pathological sections by IHC. COX-2 expression in ESCC cells was significantly increased following treatment with PAF and n-BT. Increased production of PGE2 was detected in the culture media, and the secreted PGE2 in the culture media was proportional to the increased COX-2 expression. The addition of IL-6 could also enhance COX-2 expression in ESCC cells. While NSAIDs could inhibit enzymatic activity of COX-2, they did not inhibit COX-2 gene expression in ESCC cells. PKC inhibitor, however, could abrogate PMA-induced COX-2 gene expression, but it did not block IL-6-induced COX-2 expression. Conclusions: Our data suggest that COX-2 expression in ESCC cells could be upregulated by PMA, PAF, n-BT and IL-6. Nonetheless, IL-6-induced COX-2 expression could be independent of PKC activation.

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