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Evidence for the role of 34‐kDa galactoside‐binding lectin in transformation and metastasis
Author(s) -
Raz Avraham,
Zhu Daguang,
Hogan Victor,
Shah Nipa,
Raz Tirza,
Karkash Rivka,
Pazerini Galit,
Carmi Pnina
Publication year - 1990
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.2910460520
Subject(s) - fibrosarcoma , in vitro , metastasis , in vivo , lectin , transformation (genetics) , transfection , malignant transformation , cancer research , biology , recombinant dna , neoplastic transformation , cell culture , cancer , pathology , microbiology and biotechnology , immunology , carcinogenesis , medicine , biochemistry , genetics , gene
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 .