A parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 by retinoic acid in mouse embryonal carcinoma F9 cells

Yi Lu, Brad Amos, Elizabeth Cruise, Dafna Lotan, Reuben Lotan

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Soluble endogenous lactoside-binding lectins, galectins, have been implicated in cell adhesion, growth, differentiation, neoplastic transformation, and metastasis. Two major classes of these lectins, galectin-1 and galectin-3, are developmentally regulated. To explore the mechanisms by which the expression of the galectins is regulated and to examine their association with the differentiation processes induced by all-trans retinoic acid (RA), dibutyryl cyclic AMP (Bt2cAMP) and their combination, we used the murine embryonal carcinoma (EC) cell line F9 and its RA-resistant mutant, RA-3-10. RA induced endodermal differentiation and a concurrent induction of galectin-1 and its complementary glycoconjugates (laminin and lysosomal-associated membrane protein, LAMP) in the F9 wild-type (wt) line, but failed to induce differentiation and had no effects on or even reduced the expression of galectin-1, laminin, and LAMP in the RA-3-10 line. On the other hand, RA inhibited expression of galectin-3 in the wild-type line but had no effect on the RA-3-10 line. The galectin-1 gene is at least partially regulated at the transcriptional level. These results demonstrate a parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 in F9 cells by RA. The study suggests that a regulated expression of galectins and their complementary glycoconjugates is involved in the differentiation pathway induced by RA in F9 cells.

Original languageEnglish (US)
Pages (from-to)1323-1331
Number of pages9
JournalBiological Chemistry
Volume379
Issue number11
DOIs
StatePublished - Jan 1 1998

Fingerprint

Galectin 1
Galectin 3
Embryonal Carcinoma Stem Cells
Tretinoin
Galectins
Lysosome-Associated Membrane Glycoproteins
Glycoconjugates
Laminin
Lectins
Bucladesine
Cell adhesion
Cell Adhesion
Genes
Cells
Neoplasm Metastasis

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Clinical Biochemistry

Cite this

A parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 by retinoic acid in mouse embryonal carcinoma F9 cells. / Lu, Yi; Amos, Brad; Cruise, Elizabeth; Lotan, Dafna; Lotan, Reuben.

In: Biological Chemistry, Vol. 379, No. 11, 01.01.1998, p. 1323-1331.

Research output: Contribution to journalArticle

@article{74a711007ef44d75ad3499b67c195bbe,
title = "A parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 by retinoic acid in mouse embryonal carcinoma F9 cells",
abstract = "Soluble endogenous lactoside-binding lectins, galectins, have been implicated in cell adhesion, growth, differentiation, neoplastic transformation, and metastasis. Two major classes of these lectins, galectin-1 and galectin-3, are developmentally regulated. To explore the mechanisms by which the expression of the galectins is regulated and to examine their association with the differentiation processes induced by all-trans retinoic acid (RA), dibutyryl cyclic AMP (Bt2cAMP) and their combination, we used the murine embryonal carcinoma (EC) cell line F9 and its RA-resistant mutant, RA-3-10. RA induced endodermal differentiation and a concurrent induction of galectin-1 and its complementary glycoconjugates (laminin and lysosomal-associated membrane protein, LAMP) in the F9 wild-type (wt) line, but failed to induce differentiation and had no effects on or even reduced the expression of galectin-1, laminin, and LAMP in the RA-3-10 line. On the other hand, RA inhibited expression of galectin-3 in the wild-type line but had no effect on the RA-3-10 line. The galectin-1 gene is at least partially regulated at the transcriptional level. These results demonstrate a parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 in F9 cells by RA. The study suggests that a regulated expression of galectins and their complementary glycoconjugates is involved in the differentiation pathway induced by RA in F9 cells.",
author = "Yi Lu and Brad Amos and Elizabeth Cruise and Dafna Lotan and Reuben Lotan",
year = "1998",
month = "1",
day = "1",
doi = "10.1515/bchm.1998.379.11.1323",
language = "English (US)",
volume = "379",
pages = "1323--1331",
journal = "Biological Chemistry",
issn = "1431-6730",
publisher = "Walter de Gruyter GmbH & Co. KG",
number = "11",

}

TY - JOUR

T1 - A parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 by retinoic acid in mouse embryonal carcinoma F9 cells

AU - Lu, Yi

AU - Amos, Brad

AU - Cruise, Elizabeth

AU - Lotan, Dafna

AU - Lotan, Reuben

PY - 1998/1/1

Y1 - 1998/1/1

N2 - Soluble endogenous lactoside-binding lectins, galectins, have been implicated in cell adhesion, growth, differentiation, neoplastic transformation, and metastasis. Two major classes of these lectins, galectin-1 and galectin-3, are developmentally regulated. To explore the mechanisms by which the expression of the galectins is regulated and to examine their association with the differentiation processes induced by all-trans retinoic acid (RA), dibutyryl cyclic AMP (Bt2cAMP) and their combination, we used the murine embryonal carcinoma (EC) cell line F9 and its RA-resistant mutant, RA-3-10. RA induced endodermal differentiation and a concurrent induction of galectin-1 and its complementary glycoconjugates (laminin and lysosomal-associated membrane protein, LAMP) in the F9 wild-type (wt) line, but failed to induce differentiation and had no effects on or even reduced the expression of galectin-1, laminin, and LAMP in the RA-3-10 line. On the other hand, RA inhibited expression of galectin-3 in the wild-type line but had no effect on the RA-3-10 line. The galectin-1 gene is at least partially regulated at the transcriptional level. These results demonstrate a parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 in F9 cells by RA. The study suggests that a regulated expression of galectins and their complementary glycoconjugates is involved in the differentiation pathway induced by RA in F9 cells.

AB - Soluble endogenous lactoside-binding lectins, galectins, have been implicated in cell adhesion, growth, differentiation, neoplastic transformation, and metastasis. Two major classes of these lectins, galectin-1 and galectin-3, are developmentally regulated. To explore the mechanisms by which the expression of the galectins is regulated and to examine their association with the differentiation processes induced by all-trans retinoic acid (RA), dibutyryl cyclic AMP (Bt2cAMP) and their combination, we used the murine embryonal carcinoma (EC) cell line F9 and its RA-resistant mutant, RA-3-10. RA induced endodermal differentiation and a concurrent induction of galectin-1 and its complementary glycoconjugates (laminin and lysosomal-associated membrane protein, LAMP) in the F9 wild-type (wt) line, but failed to induce differentiation and had no effects on or even reduced the expression of galectin-1, laminin, and LAMP in the RA-3-10 line. On the other hand, RA inhibited expression of galectin-3 in the wild-type line but had no effect on the RA-3-10 line. The galectin-1 gene is at least partially regulated at the transcriptional level. These results demonstrate a parallel association between differentiation and induction of galectin-1, and inhibition of galectin-3 in F9 cells by RA. The study suggests that a regulated expression of galectins and their complementary glycoconjugates is involved in the differentiation pathway induced by RA in F9 cells.

UR - http://www.scopus.com/inward/record.url?scp=0031760137&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031760137&partnerID=8YFLogxK

U2 - 10.1515/bchm.1998.379.11.1323

DO - 10.1515/bchm.1998.379.11.1323

M3 - Article

VL - 379

SP - 1323

EP - 1331

JO - Biological Chemistry

JF - Biological Chemistry

SN - 1431-6730

IS - 11

ER -