Interleukin-6 inhibits radiation induced apoptosis in pancreatic cancer cells

Y. Miyamoto, R. Hosotani, R. Doi, M. Wada, J. Ida, Shoichiro Tsuji, M. Kawaguchi, S. Nakajima, H. Kobayashi, T. Masui, M. Imamura

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Abstract

We have examined the relationship between the expression and activation of the IL-6 receptor and the possible involvement of IL-6 in the resistance of radiation-induced apoptosis in pancreatic cancer cells. Levels of IL-6 in the incubation media measured with ELISA were 1900 pg/ml in CFPAC-1, 54 pg/ml in HPAC and less than 0.2 pg/ml in MIAPaCa-2 and AsPC-1. Western blot demonstrated gp80 protein (IL-6 receptor α subunit) in all pancreatic cancer cell lines except in AsPC-1. When immunoprecipitation was performed, the bands indicating phosphorylated gp130 (IL-6R β) were observed in CFPAC-1 and HPAC, however, no band was found in MIAPaCa-2 or in AsPC-1 cells. RT-PCR and Western blot demonstrated that mRNA and protein expression for Bcl-2 and Bcl-XL was substantially increased by the IL-6 treatment in CFPAC-1 cells, but not in AsPC-1 cells. Neither exogenous IL-6 nor neutralizing anti-IL-6 mAb affected the proliferation of CFPAC-1 and AsPC-1 cells. However, the IL-6 treatment significantly attenuated the susceptibility to radiation in CFPAC-1 cells but not in AsPC-1 cells, and the neutralizing anti-IL-6 mAb significantly increased the radiosensitivity of CFPAC-1 cells. The results indicated that IL-6 might be produced in a paracrine and/or autocrine fashion in pancreatic cancer cells. II-6 inhibits radiation-induced apoptosis and enhances the survival of the cells through a functional receptor system, which is associated with the up-regulation of anti-apoptotic Bcl-2 family proteins, especially Bcl-XL.

Original languageEnglish
Pages (from-to)2449-2456
Number of pages8
JournalAnticancer Research
Volume21
Issue number4 A
Publication statusPublished - 24-11-2001

Fingerprint

Pancreatic Neoplasms
Interleukin-6
Radiation
Apoptosis
Interleukin-6 Receptors
bcl-X Protein
Western Blotting
Radiation Tolerance
Immunoprecipitation
Cell Survival
Proteins
Up-Regulation
Enzyme-Linked Immunosorbent Assay
Cell Line
Polymerase Chain Reaction
Messenger RNA
Therapeutics

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Miyamoto, Y., Hosotani, R., Doi, R., Wada, M., Ida, J., Tsuji, S., ... Imamura, M. (2001). Interleukin-6 inhibits radiation induced apoptosis in pancreatic cancer cells. Anticancer Research, 21(4 A), 2449-2456.
Miyamoto, Y. ; Hosotani, R. ; Doi, R. ; Wada, M. ; Ida, J. ; Tsuji, Shoichiro ; Kawaguchi, M. ; Nakajima, S. ; Kobayashi, H. ; Masui, T. ; Imamura, M. / Interleukin-6 inhibits radiation induced apoptosis in pancreatic cancer cells. In: Anticancer Research. 2001 ; Vol. 21, No. 4 A. pp. 2449-2456.
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Miyamoto, Y, Hosotani, R, Doi, R, Wada, M, Ida, J, Tsuji, S, Kawaguchi, M, Nakajima, S, Kobayashi, H, Masui, T & Imamura, M 2001, 'Interleukin-6 inhibits radiation induced apoptosis in pancreatic cancer cells', Anticancer Research, vol. 21, no. 4 A, pp. 2449-2456.

Interleukin-6 inhibits radiation induced apoptosis in pancreatic cancer cells. / Miyamoto, Y.; Hosotani, R.; Doi, R.; Wada, M.; Ida, J.; Tsuji, Shoichiro; Kawaguchi, M.; Nakajima, S.; Kobayashi, H.; Masui, T.; Imamura, M.

In: Anticancer Research, Vol. 21, No. 4 A, 24.11.2001, p. 2449-2456.

Research output: Contribution to journalArticle

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AU - Miyamoto, Y.

AU - Hosotani, R.

AU - Doi, R.

AU - Wada, M.

AU - Ida, J.

AU - Tsuji, Shoichiro

AU - Kawaguchi, M.

AU - Nakajima, S.

AU - Kobayashi, H.

AU - Masui, T.

AU - Imamura, M.

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N2 - We have examined the relationship between the expression and activation of the IL-6 receptor and the possible involvement of IL-6 in the resistance of radiation-induced apoptosis in pancreatic cancer cells. Levels of IL-6 in the incubation media measured with ELISA were 1900 pg/ml in CFPAC-1, 54 pg/ml in HPAC and less than 0.2 pg/ml in MIAPaCa-2 and AsPC-1. Western blot demonstrated gp80 protein (IL-6 receptor α subunit) in all pancreatic cancer cell lines except in AsPC-1. When immunoprecipitation was performed, the bands indicating phosphorylated gp130 (IL-6R β) were observed in CFPAC-1 and HPAC, however, no band was found in MIAPaCa-2 or in AsPC-1 cells. RT-PCR and Western blot demonstrated that mRNA and protein expression for Bcl-2 and Bcl-XL was substantially increased by the IL-6 treatment in CFPAC-1 cells, but not in AsPC-1 cells. Neither exogenous IL-6 nor neutralizing anti-IL-6 mAb affected the proliferation of CFPAC-1 and AsPC-1 cells. However, the IL-6 treatment significantly attenuated the susceptibility to radiation in CFPAC-1 cells but not in AsPC-1 cells, and the neutralizing anti-IL-6 mAb significantly increased the radiosensitivity of CFPAC-1 cells. The results indicated that IL-6 might be produced in a paracrine and/or autocrine fashion in pancreatic cancer cells. II-6 inhibits radiation-induced apoptosis and enhances the survival of the cells through a functional receptor system, which is associated with the up-regulation of anti-apoptotic Bcl-2 family proteins, especially Bcl-XL.

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Miyamoto Y, Hosotani R, Doi R, Wada M, Ida J, Tsuji S et al. Interleukin-6 inhibits radiation induced apoptosis in pancreatic cancer cells. Anticancer Research. 2001 Nov 24;21(4 A):2449-2456.