Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction of tumor cells with laminin is thought to be critical in invasion and metastasis. We found that an endogenous lectin, carbohydrate-binding protein 35 (CBP-35), is the major laminin-binding protein on human colon carcinoma cells and that its surface expression suggests involvement in metastasis. We identified CBP-35 by laminin-affinity chromatography and immunoblotting. Surface expression of CBP-35 on eight human colon carcinoma cell lines was compared by flow cytometry. Poorly differentiated cell lines and DLD-2, a signet-ring carcinoma cell line, expressed more surface CBP-35 than well-differentiated cell lines. Poorly differentiated cell lines and DLD-2 are characterized as aggressive cell lines because they adhere to and invade through reconstituted basement membrane significantly better than well-differentiated cell lines. These data suggest that CBP-35 is involved in tumor cell-basement membrane interactions and that an increase in CBP-35 surface expression may facilitate metastatic potential of colon carcinoma cells.
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PMID:Carbohydrate-binding protein 35 is the major cell-surface laminin-binding protein in colon carcinoma. 184 79

We previously found that galectin-3 enhanced DLD-1 cell migration through the K-Ras-Raf-Erk1/2 pathway, but the effect of extracellular galectin-3 on cancer cell migration and its interaction with the epidermal growth factor receptor (EGFR) remained unknown. We aimed to determine the effect of extracellular galectin-3 on colon cancer cell migration and its correlation with the EGFR expression. Western blotting was performed to analyze galectin-3 secretion, shRNA was used to stably knock down galectin-3 expression and a migration assay was performed to evaluate colon cancer cell migration. Tissues from eighty patients with four different stages of colon cancer were obtained and compared to normal colon tissue. The galectin-3 knockdown colon cancer cells exhibited decreased migration, which was restored by recombinant galectin-3. An EGFR blocking antibody decreased colon cancer cell migration. The addition of recombinant galectin-3 increased phosphorylated EGFR expression within minutes and enhanced the internalization of the EGFR from the cell membrane to the cytoplasm, particularly upon EGF stimulation. Extracellular galectin-3 increased colon cancer cell migration, which correlated with the EGFR. Targeting galectin-3 may have a synergistic effect on EGFR-targeted therapy.
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PMID:Extracellular galectin-3 facilitates colon cancer cell migration and is related to the epidermal growth factor receptor. 3021 Jun 79