Expression of IL-6 receptor in pancreatic cancer: Involvement in VEGF induction

Toshihiko Masui, Ryo Hosotani, Ryuichiro Doi, Yoshiharu Miyamoto, Shoichiro Tsuji, Sanae Nakajima, Hiroyuki Kobayashi, Masayuki Koizumi, Eiji Toyoda, Sidhartha Sin Tulachan, Masayuki Imamura

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Background: Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic growth factors and its expression is correlated with MVD (microvascular density) in malignant tumors, including pancreatic adenocarcinoma. On the other hand, serum interleukin-6 (IL-6) is elevated in many patients with pancreatic cancer in accordance with their disease progression. In this study, we examined whether IL-6 and its receptors have any involvement in the induction of VEGF in pancreatic cancer. Materials and Methods: Two human pancreatic cancer cell lines were examined for the induction of VEGF after treatment with IL-6. Thirty-two pancreatic cancer surgical specimens were stained immunohistochemically with VEGF, IL-6 and IL-6 receptor antibodies. Results: CFPAC-1 cells expressed IL-6 receptor whereas AsPC-1 cells rarely expressed it. IL-6 treatment induced VEGF expression significantly and dose-dependently in CFPAC-1 cells, while it did not change in AsPC-1 cells. The intensity of VEGF expression in CFPAC-1 also increased time-dependently with IL-6 treatment. In 32 surgical pancreatic cancer tissues, 19 (59%) stained positive for VEGF and 26 (87%) positive for IL-6 receptor β subunit. The correlation between IL-6 receptors and VEGF was significant (p = 0.0002 and p = 0.0019) while less correlation was seen between IL-6 and VEGF (p = 0.1937). Conclusion: Our results suggest that IL-6 is likely to take part in VEGF expression in both paracrine and autocrine fashion in pancreatic cancer. Induction of VEGF seems to be regulated by the extent of the IL-6 receptor expression on cancer cells.

Original languageEnglish
Pages (from-to)4093-4100
Number of pages8
JournalAnticancer Research
Volume22
Issue number6 C
Publication statusPublished - 01-11-2002

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Interleukin-6 Receptors
Pancreatic Neoplasms
Vascular Endothelial Growth Factor A
Interleukin-6
Angiogenesis Inducing Agents
Disease Progression
Neoplasms
Intercellular Signaling Peptides and Proteins
Adenocarcinoma
Therapeutics

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Masui, T., Hosotani, R., Doi, R., Miyamoto, Y., Tsuji, S., Nakajima, S., ... Imamura, M. (2002). Expression of IL-6 receptor in pancreatic cancer: Involvement in VEGF induction. Anticancer Research, 22(6 C), 4093-4100.
Masui, Toshihiko ; Hosotani, Ryo ; Doi, Ryuichiro ; Miyamoto, Yoshiharu ; Tsuji, Shoichiro ; Nakajima, Sanae ; Kobayashi, Hiroyuki ; Koizumi, Masayuki ; Toyoda, Eiji ; Tulachan, Sidhartha Sin ; Imamura, Masayuki. / Expression of IL-6 receptor in pancreatic cancer : Involvement in VEGF induction. In: Anticancer Research. 2002 ; Vol. 22, No. 6 C. pp. 4093-4100.
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abstract = "Background: Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic growth factors and its expression is correlated with MVD (microvascular density) in malignant tumors, including pancreatic adenocarcinoma. On the other hand, serum interleukin-6 (IL-6) is elevated in many patients with pancreatic cancer in accordance with their disease progression. In this study, we examined whether IL-6 and its receptors have any involvement in the induction of VEGF in pancreatic cancer. Materials and Methods: Two human pancreatic cancer cell lines were examined for the induction of VEGF after treatment with IL-6. Thirty-two pancreatic cancer surgical specimens were stained immunohistochemically with VEGF, IL-6 and IL-6 receptor antibodies. Results: CFPAC-1 cells expressed IL-6 receptor whereas AsPC-1 cells rarely expressed it. IL-6 treatment induced VEGF expression significantly and dose-dependently in CFPAC-1 cells, while it did not change in AsPC-1 cells. The intensity of VEGF expression in CFPAC-1 also increased time-dependently with IL-6 treatment. In 32 surgical pancreatic cancer tissues, 19 (59{\%}) stained positive for VEGF and 26 (87{\%}) positive for IL-6 receptor β subunit. The correlation between IL-6 receptors and VEGF was significant (p = 0.0002 and p = 0.0019) while less correlation was seen between IL-6 and VEGF (p = 0.1937). Conclusion: Our results suggest that IL-6 is likely to take part in VEGF expression in both paracrine and autocrine fashion in pancreatic cancer. Induction of VEGF seems to be regulated by the extent of the IL-6 receptor expression on cancer cells.",
author = "Toshihiko Masui and Ryo Hosotani and Ryuichiro Doi and Yoshiharu Miyamoto and Shoichiro Tsuji and Sanae Nakajima and Hiroyuki Kobayashi and Masayuki Koizumi and Eiji Toyoda and Tulachan, {Sidhartha Sin} and Masayuki Imamura",
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Masui, T, Hosotani, R, Doi, R, Miyamoto, Y, Tsuji, S, Nakajima, S, Kobayashi, H, Koizumi, M, Toyoda, E, Tulachan, SS & Imamura, M 2002, 'Expression of IL-6 receptor in pancreatic cancer: Involvement in VEGF induction', Anticancer Research, vol. 22, no. 6 C, pp. 4093-4100.

Expression of IL-6 receptor in pancreatic cancer : Involvement in VEGF induction. / Masui, Toshihiko; Hosotani, Ryo; Doi, Ryuichiro; Miyamoto, Yoshiharu; Tsuji, Shoichiro; Nakajima, Sanae; Kobayashi, Hiroyuki; Koizumi, Masayuki; Toyoda, Eiji; Tulachan, Sidhartha Sin; Imamura, Masayuki.

In: Anticancer Research, Vol. 22, No. 6 C, 01.11.2002, p. 4093-4100.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Expression of IL-6 receptor in pancreatic cancer

T2 - Involvement in VEGF induction

AU - Masui, Toshihiko

AU - Hosotani, Ryo

AU - Doi, Ryuichiro

AU - Miyamoto, Yoshiharu

AU - Tsuji, Shoichiro

AU - Nakajima, Sanae

AU - Kobayashi, Hiroyuki

AU - Koizumi, Masayuki

AU - Toyoda, Eiji

AU - Tulachan, Sidhartha Sin

AU - Imamura, Masayuki

PY - 2002/11/1

Y1 - 2002/11/1

N2 - Background: Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic growth factors and its expression is correlated with MVD (microvascular density) in malignant tumors, including pancreatic adenocarcinoma. On the other hand, serum interleukin-6 (IL-6) is elevated in many patients with pancreatic cancer in accordance with their disease progression. In this study, we examined whether IL-6 and its receptors have any involvement in the induction of VEGF in pancreatic cancer. Materials and Methods: Two human pancreatic cancer cell lines were examined for the induction of VEGF after treatment with IL-6. Thirty-two pancreatic cancer surgical specimens were stained immunohistochemically with VEGF, IL-6 and IL-6 receptor antibodies. Results: CFPAC-1 cells expressed IL-6 receptor whereas AsPC-1 cells rarely expressed it. IL-6 treatment induced VEGF expression significantly and dose-dependently in CFPAC-1 cells, while it did not change in AsPC-1 cells. The intensity of VEGF expression in CFPAC-1 also increased time-dependently with IL-6 treatment. In 32 surgical pancreatic cancer tissues, 19 (59%) stained positive for VEGF and 26 (87%) positive for IL-6 receptor β subunit. The correlation between IL-6 receptors and VEGF was significant (p = 0.0002 and p = 0.0019) while less correlation was seen between IL-6 and VEGF (p = 0.1937). Conclusion: Our results suggest that IL-6 is likely to take part in VEGF expression in both paracrine and autocrine fashion in pancreatic cancer. Induction of VEGF seems to be regulated by the extent of the IL-6 receptor expression on cancer cells.

AB - Background: Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic growth factors and its expression is correlated with MVD (microvascular density) in malignant tumors, including pancreatic adenocarcinoma. On the other hand, serum interleukin-6 (IL-6) is elevated in many patients with pancreatic cancer in accordance with their disease progression. In this study, we examined whether IL-6 and its receptors have any involvement in the induction of VEGF in pancreatic cancer. Materials and Methods: Two human pancreatic cancer cell lines were examined for the induction of VEGF after treatment with IL-6. Thirty-two pancreatic cancer surgical specimens were stained immunohistochemically with VEGF, IL-6 and IL-6 receptor antibodies. Results: CFPAC-1 cells expressed IL-6 receptor whereas AsPC-1 cells rarely expressed it. IL-6 treatment induced VEGF expression significantly and dose-dependently in CFPAC-1 cells, while it did not change in AsPC-1 cells. The intensity of VEGF expression in CFPAC-1 also increased time-dependently with IL-6 treatment. In 32 surgical pancreatic cancer tissues, 19 (59%) stained positive for VEGF and 26 (87%) positive for IL-6 receptor β subunit. The correlation between IL-6 receptors and VEGF was significant (p = 0.0002 and p = 0.0019) while less correlation was seen between IL-6 and VEGF (p = 0.1937). Conclusion: Our results suggest that IL-6 is likely to take part in VEGF expression in both paracrine and autocrine fashion in pancreatic cancer. Induction of VEGF seems to be regulated by the extent of the IL-6 receptor expression on cancer cells.

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Masui T, Hosotani R, Doi R, Miyamoto Y, Tsuji S, Nakajima S et al. Expression of IL-6 receptor in pancreatic cancer: Involvement in VEGF induction. Anticancer Research. 2002 Nov 1;22(6 C):4093-4100.