β Scribed by D. Dus; H. Debray; L. strzadala; J. Rak; H. Kusnierczyk; J. Montreuil; C. Radzikowski
No coin nor oath required. For personal study only.
The availability of lectin-resistant cell lines with altered carbohydrate moieties in cell surface glycoproteins and glycolipids has greatly facilitated study of the involvement of cellular glycoconjugates in tumor growth and metastasis. We present here a new animal model for metastasis study based on mouse Lewis lung carcinoma LL 2 in vitro cell line [10]. From this line, five lectin-resistant variant sublines were selected with the following lectins: wheat germ agglutinin (WGAR), Ricinus communis agglutinin II (RCA II R) and Aleuria aurantia agglutinin (AAAR). The correlation of the lectin resistance with their in vitro and in vivo growth properties, and especially lung colonizing ability, were investigated. Three WGA R variants with well-preserved tumorigenicity revealed reduced metastatic ability, both spontaneous, after subcutaneous (s.c.) administration and experimental, after intravenous (i.v.) administration. The RCA II R variant also possessed reduced spontaneous and experimental metastatic ability, but exhibited higher growth rate of local s.c. tumors. The AAA R variant possessed reduced spontaneous metastatic ability but its ability to colonize the lungs after i.v. administration was five-fold higher than that of the parent LL 2 line, whereas its tumorigenicity remained unchanged. The relative differences among WGA R variants and parent LL 2 line, concerning their experimental metastatic ability, remained similar in cyclophosphamide-modified mice to those in normal recipients.
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## Abstract From C57BL mouse melanoma Bβ16 cells, variant clones were selected __in vitro__ which were resistant to the lectins wheatβgerm agglutinin and ricin. Cells were also selected which survived toxic concentrations of concanavalin A. Four different __In vivo__ assays using intradermal, intra