A Parallel Association between Differentiation and Induction of Galectin-1, and Inhibition of Galectin-3 by Retinoic Acid in Mouse Embryonal Carcinoma F9 Cells

Lü, Yi; Amos, Brad; Cruise, Elizabeth; Lotan, Dafna; Lotan, Reuben

doi:10.1515/bchm.1998.379.11.1323

Cited by 13 publications

(8 citation statements)

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“…Previous work has provided evidence that proteins within the galectin family can be regulated by O-GlcNAcylation [17,21,22]. Few studies have examined galectins in F9 cells [40,41], where we saw no changes in Lgal3 expression in F9 cell XEN differentiation (Supplementary Materials, Figure S2); however, we observed a decrease in Lgals3 expression in terminally differentiated XEN cells compared to ES cells (Figure 3). Unlike the changes in O-GlcNAc levels, which are consistent in many previous reports [15,17,18,21], galectins appear to have context-specific changes in expression, as evident from our own studies [17,20,38].…”

Section: Discussionmentioning

confidence: 50%

O-GlcNAcylation and Regulation of Galectin-3 in Extraembryonic Endoderm Differentiation

et al. 2022

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The regulation of proteins through the addition and removal of O-linked β-N-acetylglucosamine (O-GlcNAc) plays a role in many signaling events, specifically in stem cell pluripotency and the regulation of differentiation. However, these post-translational modifications have not been explored in extraembryonic endoderm (XEN) differentiation. Of the plethora of proteins regulated through O-GlcNAc, we explored galectin-3 as a candidate protein known to have various intracellular and extracellular functions. Based on other studies, we predicted a reduction in global O-GlcNAcylation levels and a distinct galectin expression profile in XEN cells relative to embryonic stem (ES) cells. By conducting dot blot analysis, XEN cells had decreased levels of global O-GlcNAc than ES cells, which reflected a disbalance in the expression of genes encoding O-GlcNAc cycle enzymes. Immunoassays (Western blot and ELISA) revealed that although XEN cells (low O-GlcNAc) had lower concentrations of both intracellular and extracellular galectin-3 than ES cells (high O-GlcNAc), the relative secretion of galectin-3 was significantly increased by XEN cells. Inducing ES cells toward XEN in the presence of an O-GlcNAcase inhibitor was not sufficient to inhibit XEN differentiation. However, global O-GlcNAcylation was found to decrease in differentiated cells and the extracellular localization of galectin-3 accompanies these changes. Inhibiting global O-GlcNAcylation status does not, however, impact pluripotency and the ability of ES cells to differentiate to the XEN lineage.

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Section: Discussionmentioning

confidence: 50%

O-GlcNAcylation and Regulation of Galectin-3 in Extraembryonic Endoderm Differentiation

et al. 2022

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“…Spp2 transcripts have been detected in the yolk sac (Hou et al, 2007), while Galectin-1 (LGALS1) is a β-galactoside binding lectin protein that regulates MAPK signaling in various cellular contexts (Brandt et al, 2010; Thijssen et al, 2010). The expression of LGALS1 has not been reported in vivo in the extraembryonic endoderm, but it was previously reported to be activated after retinoic acid induced endodermal differentiation of F9 embryonal carcinoma cells (Lu et al, 1998). WAP four-disulfide core domain 1 (WFDC1, also referred as PS20) was identified as a prostate secreted protein with a putative serine protease inhibitor activity.…”

Section: Resultsmentioning

confidence: 99%

BMP4 signaling directs primitive endoderm-derived XEN cells to an extraembryonic visceral endoderm identity

Artus

Douvaras

Piliszek

et al. 2012

Developmental Biology

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The visceral endoderm (VE) is an epithelial tissue in the early postimplantation mouse embryo that encapsulates the pluripotent epiblast distally and the extraembryonic ectoderm proximally. In addition to facilitating nutrient exchange before the establishment of a circulation, the VE is critical for patterning the epiblast. Since VE is derived from the primitive endoderm (PrE) of the blastocyst, and PrE-derived eXtraembryonic ENdoderm (XEN) cells can be propagated in vitro, XEN cells should provide an important tool for identifying factors that direct VE differentiation. In this study, we demonstrated that BMP4 signalling induces the formation of a polarized epithelium in XEN cells. This morphological transition was reversible, and was associated with the acquisition of a molecular signature comparable to extraembryonic (ex) VE. Resembling exVE which will form the endoderm of the visceral yolk sac, BMP4-treated XEN cells regulated hematopoiesis by stimulating the expansion of primitive erythroid progenitors. We also observed that LIF exerted an antagonistic effect on BMP4-induced XEN cell differentiation, thereby impacting the extrinsic conditions used for the isolation and maintenance of XEN cells in an undifferentiated state. Taken together, our data suggest that XEN cells can be differentiated towards an exVE identity upon BMP4 stimulation, and therefore represent a valuable tool for investigating PrE lineage differentiation.

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“…Recently, a study from our group showed that melanocytes accumulate galectin-3 with tumor progression (27). Earlier, our group has also shown that retinoic acid inhibits the expression of galectin-3 and causes differentiation in mouse embryonal carcinoma F9 cells (28).…”

Section: Discussionmentioning

confidence: 94%

Decreased Expression of Retinoid Receptors in Melanoma: Entailment in Tumorigenesis and Prognosis

Chakravarti¹,

Lotan²,

Diwan³

et al. 2007

Clinical Cancer Research

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Purpose: Retinoids inhibit proliferation and induce differentiation in melanoma cells. Retinoic acid receptors (RAR) and retinoid X receptors (RXR) mediate the various modulatory effects of retinoids in cells. We have studied the in situ expression of each RAR and RXR protein (a, h, g) in a large series of melanocytic lesions and correlated the expression with clinicopathologic features and prognosis of the patients. Experimental Design:Tissue microarray blocks of 226 melanocytic lesions were semiquantitatively evaluated by immunohistochemistry for the cytoplasmic and nuclear expression of RAR and RXR protein (a, h, g).Results: A significant decrease of RARh protein (P < 0.0001), nuclear expression of RARg (P < 0.0001), and RXRa (P < 0.0001) was found in primary and metastatic melanomas as compared with nevi. Loss of nuclear immunoreactivity for RARg (P = 0.048) and RXRa (P = 0.001) was observed in the lesions showing vertical growth pattern. In addition, in patients with concomitant loss of cytoplasmic staining for RARa and RXRa, the probability of overall survival (log-rank test, P = 0.002) and disease-specific survival (log-rank test, P = 0.014) was significantly lower. Conclusions: Aberrant expression of retinoid receptors seems to be a frequent event in melanoma and suggests an impairment of the retinoid pathway in this cancer. Our data indicate the loss of retinoid receptor expression with melanoma progression and suggest a possible prognostic significance of the analysis of retinoid receptors in melanoma.

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A Parallel Association between Differentiation and Induction of Galectin-1, and Inhibition of Galectin-3 by Retinoic Acid in Mouse Embryonal Carcinoma F9 Cells

Cited by 13 publications

References 58 publications

O-GlcNAcylation and Regulation of Galectin-3 in Extraembryonic Endoderm Differentiation

O-GlcNAcylation and Regulation of Galectin-3 in Extraembryonic Endoderm Differentiation

BMP4 signaling directs primitive endoderm-derived XEN cells to an extraembryonic visceral endoderm identity

Decreased Expression of Retinoid Receptors in Melanoma: Entailment in Tumorigenesis and Prognosis

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