Different Response to Retinoic Acid of Two Teratocarcinoma Cell Lines

Yu-Jui Yvonne Wan, Lai Wang, Tsung Chieh Jackson Wu

Research output: Contribution to journalArticle

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Abstract

Retinoic acid (RA), a well-known inducer of differentiation, has been shown to regulate its own receptor gene expression in F9 teratocarcinoma cells. The homologous regulation of receptors by RA might be critical for RA-induced F9 cell differentiation. F9 cell lines from two different laboratories, named F9-1 and F9-2, were compared for retinoic acid receptor (RAR) and retinoid x receptor (RXR) gene expression in response to RA. The data show that both F9-1 and F9-2 cell lines are embryonal carcinoma cells, but of different phenotypes and different sensitivity to RA. In F9-1 cells, RA regulates all three RARs (α, β, and γ), two RXRs (α and γ), two activin receptors (ActR II and IIB), and tissue-specific plasminogen activator (t-PA) gene expression. In F9-2 cells RA regulates only the RARβ, RXRα, and t-PA genes. The induction of mRNA levels was much higher in F9-1 than in F9-2 cells. Different basal RARγ and RXRγ mRNA levels were also noted. In these two cell lines F9-2 cells expressed greater amounts of RARγ1, γ2, and γ3 mRNA isoforms, but lacked RXRγ mRNA compared with F9-1 cells. Since RARγ1 has been shown to exert an antagonistic effect on other types of RA receptors, the decreased sensitivity of F9-2 cells to RA might be due to its high level of RARγ1 and/or low level of RXRγ. This notion was in part supported by gel shift assay which demonstrated constitutive binding of RARγ to a RA responsive element (RARβE) in F9-2 cells. Further, the binding of nuclear protein to RARβE was increased upon RA treatment in F9-1 cells, but not in F9-2 cells. These differences in the regulation of RA receptors might determine the sensitivity of the two substrains of F9 cells to RA.

Original languageEnglish (US)
Pages (from-to)392-398
Number of pages7
JournalExperimental Cell Research
Volume219
Issue number2
DOIs
StatePublished - Aug 1995

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Teratocarcinoma
Tretinoin
Retinoic Acid Receptors
Cell Line
Retinoids
Tissue Plasminogen Activator
Gene Expression
Messenger RNA
Activin Receptors
RNA Isoforms
Embryonal Carcinoma Stem Cells
Nuclear Proteins
Cell Differentiation
Carrier Proteins
Gels

ASJC Scopus subject areas

  • Cell Biology

Cite this

Different Response to Retinoic Acid of Two Teratocarcinoma Cell Lines. / Wan, Yu-Jui Yvonne; Wang, Lai; Wu, Tsung Chieh Jackson.

In: Experimental Cell Research, Vol. 219, No. 2, 08.1995, p. 392-398.

Research output: Contribution to journalArticle

Wan, Yu-Jui Yvonne ; Wang, Lai ; Wu, Tsung Chieh Jackson. / Different Response to Retinoic Acid of Two Teratocarcinoma Cell Lines. In: Experimental Cell Research. 1995 ; Vol. 219, No. 2. pp. 392-398.
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abstract = "Retinoic acid (RA), a well-known inducer of differentiation, has been shown to regulate its own receptor gene expression in F9 teratocarcinoma cells. The homologous regulation of receptors by RA might be critical for RA-induced F9 cell differentiation. F9 cell lines from two different laboratories, named F9-1 and F9-2, were compared for retinoic acid receptor (RAR) and retinoid x receptor (RXR) gene expression in response to RA. The data show that both F9-1 and F9-2 cell lines are embryonal carcinoma cells, but of different phenotypes and different sensitivity to RA. In F9-1 cells, RA regulates all three RARs (α, β, and γ), two RXRs (α and γ), two activin receptors (ActR II and IIB), and tissue-specific plasminogen activator (t-PA) gene expression. In F9-2 cells RA regulates only the RARβ, RXRα, and t-PA genes. The induction of mRNA levels was much higher in F9-1 than in F9-2 cells. Different basal RARγ and RXRγ mRNA levels were also noted. In these two cell lines F9-2 cells expressed greater amounts of RARγ1, γ2, and γ3 mRNA isoforms, but lacked RXRγ mRNA compared with F9-1 cells. Since RARγ1 has been shown to exert an antagonistic effect on other types of RA receptors, the decreased sensitivity of F9-2 cells to RA might be due to its high level of RARγ1 and/or low level of RXRγ. This notion was in part supported by gel shift assay which demonstrated constitutive binding of RARγ to a RA responsive element (RARβE) in F9-2 cells. Further, the binding of nuclear protein to RARβE was increased upon RA treatment in F9-1 cells, but not in F9-2 cells. These differences in the regulation of RA receptors might determine the sensitivity of the two substrains of F9 cells to RA.",
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