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Comparison of autocrine mechanisms promoting motility in two metastatic cell lines: Human melanoma and ras ‐transfected NIH3T3 cells
Author(s) -
Seiki Motoharu,
Sato Hiroshi,
Liotta Lance A.,
Schiffmann Elliott
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.2910490515
Subject(s) - motility , transfection , autocrine signalling , pertussis toxin , biology , receptor , cell culture , microbiology and biotechnology , cell , signal transduction , g protein , biochemistry , genetics
Tumor‐cell migration plays an essential role in invasion into surrounding tissues and the formation of metastatic colonies in distant organs. Metastatic human A2058 melanoma and ras ‐ transfected NIH3T3 cells produce autocrine motility factors (AMFs) which stimulate their own motility, and the A2058 cell AMF (AMF/A2058) has been purified. In this study, we partially purified the AMF produced by N‐ras ‐transfected NIH3T3 cells (AMF/NIH3T3) and compared it with AMF/A2058. The two AMFs differed in their gel filtration patterns and heat stability, although both elicited migration of N‐ras ‐transfected NIH3T3 cells. The receptor for AMF/A2058 in A2058 cells is linked to pertussis‐toxin‐sensitive GTP‐binding protein. Pre‐treatment of N‐ras ‐transfected NIH3T3 cells with pertussis toxin also specifically blocked the promotion of motility by AMF/A2058, but did not affect the activity of AMF/NIH3T3. Stimulation of N‐ras ‐transfected NIH3T3 cells by both AMFs elicited an additive response. Thus, the autocrine mechanisms of these two metastatic tumor cell lines are different with regard to the AMF molecules, receptors, and signal transduction pathways.