Studies on the effect of retinoids on the differentiation of teratocarcinoma stem cells in vitro and in vivo

Strickland, Sidney; Sawey, Mary Jean

doi:10.1016/0012-1606(80)90319-x

Cited by 96 publications

(49 citation statements)

References 17 publications

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“…4). An increase in RAR-j3 message was not detected until 6 analyzed for RAR-p mRNA as described for Fig. 1 5-7).…”

Section: Resultsmentioning

confidence: 89%

“…The distinct patterns of expression and different affinities for retinoic acid suggest distinct roles for these receptors in the manifestation of retinoic acid action (17-19, 21, 22 (9). Differentiation is characterized by loss of tumorigenicity, decreased proliferation, and large changes in the expression of plasminogen activator, laminin, collagen IV, and c-myc product, as well as in the cell surface antigen SSEA-1 (6,(9)(10)(11). The most potent of the naturally occurring retinoids in promoting F9 cell differentiation is retinoic acid (6,9,12,13).…”

mentioning

confidence: 99%

“…Differentiation is characterized by loss of tumorigenicity, decreased proliferation, and large changes in the expression of plasminogen activator, laminin, collagen IV, and c-myc product, as well as in the cell surface antigen SSEA-1 (6,(9)(10)(11). The most potent of the naturally occurring retinoids in promoting F9 cell differentiation is retinoic acid (6,9,12,13). Retinoic acid is a physiologically occurring and activated metabolite of retinol (14) that appears to act directly in stimulating F9 cell differentiation (12).…”

mentioning

confidence: 99%

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Retinoic acid, dibutyryl-cAMP, and differentiation affect the expression of retinoic acid receptors in F9 cells.

Martin

Ziegler

Napoli

1990

Proc. Natl. Acad. Sci. U.S.A.

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Expression of the retinoic acid receptors a and (3 (RAR-a and RAR-(3) was examined in F9 cells, an embryonal carcinoma cell model established for the study of retinoid metabolism and function. Addition of retinoic acid to F9 cell medium caused a dose-dependent increase in RAR-fi mRNA within 3 hr that reached 5-to 30-fold greater than the constitutively expressed mRNA by 24 hr. ized by loss of tumorigenicity, decreased proliferation, and large changes in the expression of plasminogen activator, laminin, collagen IV, and c-myc product, as well as in the cell surface antigen SSEA-1 (6, 9-11). The most potent of the naturally occurring retinoids in promoting F9 cell differentiation is retinoic acid (6,9,12,13). Retinoic acid is a physiologically occurring and activated metabolite of retinol (14) that appears to act directly in stimulating F9 cell differentiation (12). The discovery of three distinct retinoic acid receptors, a,

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“…4). An increase in RAR-j3 message was not detected until 6 analyzed for RAR-p mRNA as described for Fig. 1 5-7).…”

Section: Resultsmentioning

confidence: 89%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Retinoic acid, dibutyryl-cAMP, and differentiation affect the expression of retinoic acid receptors in F9 cells.

Martin

Ziegler

Napoli

1990

Proc. Natl. Acad. Sci. U.S.A.

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“…Retinoids are well-known differentiation-enhancing agents and have been shown to exert antineoplastic activities in vitro against a variety of cancers, including acute promyelocytic leukaemia, germ cell tumours, breast cancer, head and neck squamous cell carcinoma, myeloma and neuroblastoma (Strickland and Sawey, 1980;Butler and Fontana, 1992;Zou et al, 1994;Cohen et al, 1995;Palumbo et al, 1995). Furthermore, all-trans retinoic acid (RA) has been used effectively in vivo to treat acute promyelocytic leukaemia patients (Huang et al, 1988;Degos, 1992;Warrell et al, 1991Warrell et al, , 1993.…”

mentioning

confidence: 99%

All-trans retinoic acid decreases susceptibility of a gastric cancer cell line to lymphokine-activated killer cytotoxicity

Chao¹,

Jiang²,

Shyu³

et al. 1997

Br J Cancer

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Summary All-trans retinoic acid (RA) was previously shown to regulate the growth of gastric cancer cells derived from the cell line SC-Mi. This study was designed to investigate the effect of RA on the sensitivity of SC-Mi cells to lymphokine-activated killer (LAK) activity. RA at the concentration range of 0.001-10 kM was shown to induce SC-Mi cells to exhibit resistance to LAK activity in a dose-dependent manner. A kinetics study indicated that a significantly increased resistance was detected after 2 days of co-culturing SC-Mi cells with RA and reached a maximum after 6 days of culture. Similar results were obtained from two other cancer cell lines: promyelocytic leukaemia HL-60 and hepatic cancer Hep 3B. A binding assay demonstrated that the binding efficacy between target SC-M1 cells and effector LAK cells was not altered by RA. Flow cytometric analyses revealed that RA exhibited no effect on the expression of cell surface molecules, including HLA class and class 11 antigens, intercellular adhesion molecule-1 and -2, and lymphocyte function antigen-3. Cell cycle analysis revealed that culture of SC-Mi cells with RA resulted in an increase in GJG, phase and a decrease in S phase, accompanied by a decrease in cyclin A and cyclin Bi mRNA as determined by Northern blot analysis. Additionally, RA was shown to enhance the expression of retinoic acid receptor a (RARa) in SC-Mi cells, and to have no effect on the expression of RARfi or RARy. Taken together, these results indicate that RA can significantly increase gastric cancer cells SC-Mi to resist LAK cytotoxicity by means of a cytostatic effect through a mechanism relating to cell cycle regulation. The prevailing ideas, such as a decrease in effector to target cell binding, a reduced MHC class antigen expression or an altered RARP expression, are not involved.

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“…PLD, phospholipase D; ARF, ADP ribosylation factor; RA, retinoic acid; dbcAMP, dibutyryl cyclic AMP; GTPTS , guanosine 5'-O-(3-thiotriphosphate); PtdBut, phosphatidylbutanol entiation agent and has been used as an anti-cancer drug. On the other hand, when RA and dibutyryl cyclic AMP (dbcAMP) are added to culture media, F9 cells differentiate into a second phenotype that morphologically and biochemically resembles parietal endoderm cells [3,4] which synthesize large quantities of extracellular matrix constituents including laminin, entactin and proteoglycan. Although the mechanism whereby RA regulates gene expression and differentiation is not completely understood, it is likely that high affinity RA receptor and/or cellular RA binding proteins are involved [5,6].…”

Section: Introductionmentioning

confidence: 99%

Down‐regulation of phospholipase D during differentiation of mouse F9 teratocarcinoma cells

et al. 1999

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Studies on the effect of retinoids on the differentiation of teratocarcinoma stem cells in vitro and in vivo

Cited by 96 publications

References 17 publications

Retinoic acid, dibutyryl-cAMP, and differentiation affect the expression of retinoic acid receptors in F9 cells.

Retinoic acid, dibutyryl-cAMP, and differentiation affect the expression of retinoic acid receptors in F9 cells.

All-trans retinoic acid decreases susceptibility of a gastric cancer cell line to lymphokine-activated killer cytotoxicity

Down‐regulation of phospholipase D during differentiation of mouse F9 teratocarcinoma cells

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