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TNF‐mediated cytotoxicity and resistance in human prostate cancer cell lines
Author(s) -
Nakajima Yosuke,
DelliPizzi Ann Marie,
Mallouh Camille,
Ferreri Nicholas R.
Publication year - 1996
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(199611)29:5<296::aid-pros4>3.0.co;2-8
Subject(s) - lncap , tumor necrosis factor alpha , cell culture , androgen receptor , prostate cancer , receptor , cancer research , cytotoxicity , endocrinology , monoclonal antibody , cell , cytokine , medicine , biology , immunology , cancer , antibody , in vitro , biochemistry , genetics
BACKGROUND The contribution of TNF receptor (TNF‐R) expression was investigated with respect to TNF sensitivity or insensitivity for androgen‐dependent and androgen‐independent human prostate cancer (PCA) cell lines, respectively. METHODS Flow cytometric analyses using monoclonal antibodies against the 55‐kDa receptor (TNF‐R1) and the 75‐kDa receptor (TNF‐R2) indicated that both receptors were expressed on all three cell lines. RESULTS Moreover, expression of TNF‐R1 was greater than expression of TNF‐R2 in these PCA cells. All three PCA cell lines produced IL‐6. However, IL‐6 production was enhanced when TNF‐insensitive JCA‐1 and PC‐3 cells, but not TNF‐sensitive LNCaP cells, were treated with rTNF (10 −9 M). CONCLUSIONS These data suggest that the lack of an antiproliferative effect of rTNF on the androgen‐independent PCA cell lines PC‐3 and JCA‐1 is not due to the failure of these cells to express TNF‐R, but may be related to the differences in TNF‐mediated IL‐6 expression by these PCA cell lines. © 1996 Wiley‐Liss, Inc.