Hormonal induction of differentiation in teratocarcinoma stem cells: Generation of parietal endoderm by retinoic acid and dibutyryl cAMP

Strickland, Sidney; Smith, Karen Kaye; Marotti, Keith R.

doi:10.1016/0092-8674(80)90471-7

Cited by 759 publications

(452 citation statements)

References 31 publications

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“…After 2 and 3 days of retinoic acid treatment, however, there is a doubling in enzyme activity. This would correspond to the results of previous studies which have described a 2-3-day lag between initial treatment of F9 cells with retinoic acid and the appearance of cells with parietal endoderm-like properties [3, 15,16]. The amount of galactosyltransferase activity was further increased in cells exposed to retinoic acid for 4 and 6 days.…”

Section: Resultssupporting

confidence: 90%

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Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F₉ embryonal carcinoma cells

1984

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Exposure of F9 cells to all-trans-retinoic acid over a period of 6 days resulted in 4-fold induction of cell surface N-acetylglucosaminide fi( l -+4)galactosyltransferase (GT) activity. The retinoic acid-induced GT activity was further enhanced by treatment of the cells with I-bromo cyclic AMP. The ability of retinoic acid alone, or retinoic acid in combination with 8-bromo cyclic AMP, to induce GT activity was inhibited by both actinomycin D and cycloheximide. These findings indicate that the induction of galactosyltransferase activity noted with differentiation of F9 cells involves de novo synthesis of new enzyme protein. F9 cell Retinoic acid 8-Bromo cyclic AMP Galactosyltransferase activity De novo synthesis

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Section: Resultssupporting

confidence: 90%

“…Cyclic AMP has been shown to promote retinoic acid-induced differentiation of F9 cells to endoderm [6,15,16]. In agreement with these studies, in F9 cells treated for 3 and 6 days with retinoic acid and for an additional 24 h with retinoic acid in the presence and absence of 8-bromo cyclic AMP, cyclic AMP elicits a further 2-fold increase 2).…”

Section: Resultssupporting

confidence: 61%

Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F₉ embryonal carcinoma cells

1984

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“…It is well known that they are involved in the normal development process. Mouse teratocarcinoma cells di erentiated into parietal endoderm-like cells upon retinoic acid treatment in vitro (Strickland et al, 1980;Sporn and Roberts, 1983;Savatier et al, 1995). Many reports demonstrated that retinoids inhibited the growth of a variety of tumors and transformed cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of cyclin D expression in human breast carcinoma cells by retinoids in vitro

1997

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Transfection and transgenic mouse experiments supported an oncogenic role for cyclin D1 in breast cancer. We recently reported that noninvasive carcinoma in situ lesions of the human breast overexpress cyclin D, suggesting that this molecular event may represent a valuable target for chemoprevention. The purpose of the present series of investigations was to identify agents which could reduce the cyclin D expression of breast cells. We report that 9-cis retinoic acid (9-cis RA) and all trans retinoic acid (tRA) inhibited the cyclin D1 and D3 expression levels of human MCF-7, ZR-75 and T-47D breast carcinoma cells in vitro. Where detectable, similar trends were observed in the immortalized, HBL-100 and MCF-10A breast cell lines. Cyclin D2 was undetectable. The e ect of retinoids was both dose-and time-dependent, and correlated with altered cell cycle kinetics and proliferative status. Retinoids were also found to inhibit the expression levels of other cell cycle related proteins, including Cdk2 and Cdk4, resulting in lower kinase activities. In contrast to other breast prevention studies, no synergistic e ect was observed with retinoids and tamoxifen. The data indicate that retinoids can potently reduce cyclin D expression levels in a variety of breast cell lines in vitro, and suggest further consideration of this mechanism for the chemoprevention of breast cancer.

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“…F9 embryonal carcinoma (EC) cells are a well-known system for extra-endoderm differentiation in early mouse embryogenesis. In the presence of retinoic acid (RA), F9 EC cells differentiate toward primitive endoderm (PrE) [16], and if dibutyryl cyclic AMP (bt 2 cAMP) is added together with the RA, the F9 EC cells differentiate to parietal endoderm (PE) via PrE [17]. We examined the expression profile for each S1P receptor throughout this differentiation.…”

Section: Introductionmentioning

confidence: 99%

Changes in S1P1 and S1P2 expression during embryonal development and primitive endoderm differentiation of F9 cells

Hiraga

Kihara

Sano

et al. 2006

Biochemical and Biophysical Research Communications

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Sphingosine 1-phosphate (S1P) is a ligand for S1P family receptors (S1P 1 -S1P 5 ).Of these receptors, S1P 1 , S1P 2 , and S1P 3 are ubiquitously expressed in adult mice, while S1P 4 and S1P 5 are tissue-specific. However, little is known of their expression during embryonal development. We performed Northern blot analyses in mouse embryonal tissue and found that such expression is developmentally regulated. We also examined the expression of these receptors during primitive endoderm (PrE) differentiation of mouse F9 embryonal carcinoma (EC) cells, a well-known in vitro endoderm differentiation system. S1P 2 mRNA was abundantly expressed in F9 EC cells, but little S1P 1 and no S1P 3 , S1P 4 , or S1P 5 mRNA was detectable. However, S1P 1 mRNA expression was induced during EC-to-PrE differentiation. Studies using small interference RNA of S1P 1 indicated that increased S1P 1 expression is required for PrE differentiation. Thus, S1P 1 may play an important function in PrE differentiation that is not substituted for by S1P 2 .

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Hormonal induction of differentiation in teratocarcinoma stem cells: Generation of parietal endoderm by retinoic acid and dibutyryl cAMP

Cited by 759 publications

References 31 publications

Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F₉ embryonal carcinoma cells

Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F₉ embryonal carcinoma cells

Inhibition of cyclin D expression in human breast carcinoma cells by retinoids in vitro

Changes in S1P1 and S1P2 expression during embryonal development and primitive endoderm differentiation of F9 cells

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Hormonal induction of differentiation in teratocarcinoma stem cells: Generation of parietal endoderm by retinoic acid and dibutyryl cAMP

Cited by 759 publications

References 31 publications

Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F9 embryonal carcinoma cells

Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F9 embryonal carcinoma cells

Inhibition of cyclin D expression in human breast carcinoma cells by retinoids in vitro

Changes in S1P1 and S1P2 expression during embryonal development and primitive endoderm differentiation of F9 cells

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Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F₉ embryonal carcinoma cells

Increase in cell‐surface N‐acetylglucosaminide β(1→4)galactosyltransferase activity with retinoic acid‐induced differentiation of F₉ embryonal carcinoma cells