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 language | English (US) |
|---|---|
| Pages (from-to) | 392-398 |
| Number of pages | 7 |
| Journal | Experimental Cell Research |
| Volume | 219 |
| Issue number | 2 |
| DOIs | |
| State | Published - Aug 1995 |
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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 journal › Article
}
TY - JOUR
T1 - Different Response to Retinoic Acid of Two Teratocarcinoma Cell Lines
AU - Wan, Yu-Jui Yvonne
AU - Wang, Lai
AU - Wu, Tsung Chieh Jackson
PY - 1995/8
Y1 - 1995/8
N2 - 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.
AB - 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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UR - http://www.scopus.com/inward/citedby.url?scp=0029090950&partnerID=8YFLogxK
U2 - 10.1006/excr.1995.1244
DO - 10.1006/excr.1995.1244
M3 - Article
C2 - 7543852
AN - SCOPUS:0029090950
VL - 219
SP - 392
EP - 398
JO - Experimental Cell Research
JF - Experimental Cell Research
SN - 0014-4827
IS - 2
ER -