Antitumor effect of interferon-α, γ and/or tumor necrosis factor-α against human colon cancer line (LoVo) transplanted into nude mice

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  • KATAOKA Kazuhiko
    First Department of Surgery, Okayama University Medical School
  • NAOMOTO Yoshio
    First Department of Surgery, Okayama University Medical School
  • MURO Masahiko
    First Department of Surgery, Okayama University Medical School
  • KOJIMA Kazushi
    First Department of Surgery, Okayama University Medical School
  • HORIKI Sadayuki
    First Department of Surgery, Okayama University Medical School
  • HIZUTA Akio
    First Department of Surgery, Okayama University Medical School
  • TANAKA Noriaki
    First Department of Surgery, Okayama University Medical School
  • ORITA Kunzo
    First Department of Surgery, Okayama University Medical School

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Other Title
  • ヌードマウス可移植性ヒト大腸癌細胞株LoVoに対するinterferon-α, -γ, tumor necrosis factor-αの抗腫瘍効果の検討
  • Antitumor effect of interferon-α, γ and/or tumor necrosis factor-α against human colon cancer line (LoVo) transplanted into nude mice

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We investigated the in vivo antitumor effect of recombinant human interferon-α, γ (IFN-α, γ) and/or recombinant human tumor necrosis factor-α (TNF-α) against human colon cancer cells (LoVo) transplanted into nude mice. LoVo cells were very sensitive to IFN-γ and slightly sensitive to IFN-α and resistant to TNF-α in vitro by dye uptake method. Intravenous administration of IFN-γ significantly inhibited tumor growth transplanted subcutaneously into nude mice, but IFN-α and/or TEN-α did not show any antitumor effect. Labeling index on staining with bromodeoxyuridine and mitotic index of LoVo cells treated with IFN-α, γ or TNF-α differed slightly from those of the control group. We previously reported that the synergistic antitumor effects on the three cell lines could be examined by the combined use of IFN-α and TNF-α and the mechanism of the synergism was arrested in the S phase of cell cycle of target cells. However in the case of LoVo cells, the combined use of IFN-α and TNF-α was not effective and did not arrest the cells in the S phase of cell cycle. Therefore, arrest in the S phase was suspected to be responsible from the synergistic antitumor activity of IFN-α and TNF-α on the sensitive targets.

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