Evidence for the role of 34‐kDa galactoside‐binding lectin in transformation and metastasis

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Abstract
The endogenous M, 34,000 galaictoside‐binding lectin (L‐34) is found at elevated levels in a wilde variety of neoplastic cells and correlative evidence suggests that it is involved in tumor metastasis in vivo and in transformation in vitro. We demonstrate here that introduction of recombinant L‐34 into tumorigenic, weakly metastatic UV‐2237‐cl‐ I 5 fibrosarcoma cells results in an increased incidence of experimental lung metastases in syngeneic and nude mice. Transfection of normal BALB/c‐A3 I cloned fibroblasts with functional L‐34 results in acquisition of anchorage‐independent growth and in morphological transformation in vitro but not in tumorigenicity in vivo. These results provide direct evidence that the cellular expression of L‐34 is associated with some aspects of transformation and with metastasis, but not with tumorigenicity per se.