Inhibition of lung colonization of mouse colon 26 adenocarcinoma by recombinant mouse interferon beta through a modification of platelet function.
Recombinant murine interferon beta (MuIFN-beta) given i.v. efficiently inhibited both pulmonary arrest and formation of lung colonies of NL-17, a highly metastatic variant of mouse colon adenocarcinoma 26. NL-17 was rather resistant to MuIFN-beta in vitro and was highly resistant to natural killer cells of mice even though they were treated in vivo with MuIFN-beta. Platelets isolated from MuIFN-beta-treated mice showed reduced aggregating activity induced by NL-17. Since lung colonization by NL-17 is influenced by platelet aggregation, the inhibition of colonization by MuIFN-beta could be partly mediated through modification of platelet function in vivo. The effect of MuIFN-beta on platelet function and its subsequent inhibition of lung colony formation give new insights into the action of recombinant MuIFN-beta.
Tsuruo
T
T
Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, Tokyo.
Saito
H
H
Watanabe
M
M
Sugimoto
Y
Y
Yamori
T
T
Oh-Hara
T
T
D000230:Adenocarcinoma / Q000473:pathology; D000818:Animals; D001792:Blood Platelets / Q000187:drug effects*; D003110:Colonic Neoplasms / Q000473:pathology; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D005260:Female; D007370:Interferon Type I / Q000494:pharmacology*; D007694:Killer Cells, Natural / Q000187:drug effects / Q000276:immunology; D008175:Lung Neoplasms / Q000517:prevention & control / Q000556:secondary*; D051379:Mice; D008815:Mice, Inbred Strains; D010974:Platelet Aggregation / Q000187:drug effects; D010976:Platelet Count; D011994:Recombinant Proteins
D007370:Interferon Type I; D011994:Recombinant Proteins