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Interferon‐gamma interrupts autocrine growth mediated by endogenous interleukin‐6 in renal‐cell carcinoma
Author(s) -
Gruss H.J.,
Brach M. A.,
Mertelsmann R. H.,
Herrmann F.
Publication year - 1991
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.2910490523
Subject(s) - autocrine signalling , cytokine , cell culture , interferon gamma , cell growth , biology , interleukin 2 , cancer research , endocrinology , medicine , immunology , biochemistry , genetics
Cells of the renal‐cell carcinoma line ACHN constitutively produce IL‐6, express the IL‐6 receptor and use IL‐6 in an autocrine fashion to augment their growth. Growth arrest of ACHN cells can be achieved by exposure of cells to neutralizing monoclonal antibody (MAb) to recombinant human (rh) IL‐6. Treatment of ACHN cells with rh IFN‐γ also leads to inhibition of proliferation of these cells in a dose‐dependent manner, that can be reversed by exogenous rh IL‐6, while IFN‐α, IL‐2, IL‐4 and vinblastine or 17‐β‐estradiol has no effect on growth ( 3 H‐thymidine uptake) of ACHN cells and IL‐6 expression. Studies on the mechanism of action of IFN‐γ revealed that IFN‐γ was acting by inhibiting the autocrine IL‐6‐mediated loop generated by ACHN.