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Enhanced metastases of a mouse carcinoma after in vitro treatment with murine interferon gamma
Author(s) -
Ramani Pijamila,
Balkwill Frances R.
Publication year - 1987
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910400621
Subject(s) - in vitro , in vivo , cancer research , antigen , ratón , biology , adenocarcinoma , interferon gamma , immunology , microbiology and biotechnology , cytokine , cancer , biochemistry , genetics
We have studied the influence of inter ferons (IFNs) on the metastatic potential of mouse colon adenocarcinoma, COLON 26, cells. Pre‐treatment of the cells in vitro for 24 hr with recombinant murine IFN‐γ (rMuIFN‐γ) significantly in‐creased the number of lung tumour nodules when cells were injected i.v. into immunocompetent BALB/c mice and BALB/ c nude mice. However when MulFN‐γ‐pre‐treated cells were injected into beige (NK‐deficient) nude mice or anti‐asialoGM I (as GMI)‐serum‐treated BALB/c mice (NK‐depleted) no enhancement of metastatic potential was seen. Pre‐treatment of COLON 26 cells with recombinant human IFN‐α A/D (Bgl I), an IFN with equal activity on human and mouse cells, did net significantly enhance their subsequent metastases in immunocompetent or immunodeficient mice. In fact, there was a small but significant decrease in the number of tumour nodules in the lungs of beige nude and asGM I ‐treated mice. The e effects of rMuIFN‐γ on COLON 26 cells did not appear to be related to an alteration in MHC expression. COLON 26 eel Is constitutively express H‐2D and H‐2K antigens and both IFNs had equal enhancing (approx. 2‐fold) activity on the expression of these antigens at the doses used in this experiment (10 3 U/ml). We conclude that pre‐treatment with rMuIFN‐γ renders COLON 26 cells resistant to in vivo NK‐cell lysis via a mechanism that does not involve changes in MHC expression.