Abstract
Retinoic acid (RA) induces apoptosis in Hep3B human hepatoma cells. 9-Cis-RA (c-RA) had a similar effect as all-trans-RA (t-RA) in inducing cell death in Hep3B cells. RA-induced Hep3B-cell death was associated with inhibited expression of the hepatocyte nuclear factor 4 (HNF-4) gene. Palmitoyl-CoA ((C16:0)-CoA), the reported HNF-4 ligand, prevented RA-induced apoptosis. The effect of (C16:0)-CoA was specific, since palmitic acid and co-enzyme A had no effect in preventing RA-induced apoptosis. Bovine serum albumin (BSA) also prevented RA-induced apoptosis. However, in contrast to BSA, which induced cell growth, (C16:0)-CoA alone had no effect on cell growth. Investigating the possible role of HNF-4 in apoptosis, the reported HNF-4 antagonist (C18:0)-CoA was employed, and it also prevented RA-induced apoptosis. By transient transfection, overexpression of HNF-4 did not prevent RA-induced apoptosis. The induction and prevention of apoptosis caused by RA and (C16:0)-CoA were associated, respectively with the induction and inhibition of the expression of transforming growth factor β (TGFβ), which is known to play a role in apoptosis. Furthermore, RA and (C16:0)-CoA can regulate AP-1, which is a key regulator of the TGFβ gene. Our data indicate that fatty acyl-CoAs can prevent RA-induced apoptosis and that TGFβ, rather than HNF-4, may play a role in these regulatory processes. Our data also suggest that (C16:0)-CoA and (C18:0)-CoA are not the agonist and antagonist for HNF4, respectively in the Hep3B cell system. Copyright (C) 2000 Elsevier Science Ireland Ltd.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 19-27 |
| Number of pages | 9 |
| Journal | Cancer Letters |
| Volume | 154 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jun 1 2000 |
Fingerprint
Keywords
- Apoptosis
- Fatty acyl-CoA
- Hepatocyte nuclear factor 4
- Hepatoma
- Retinoic acid
- Transforming growth factor β
ASJC Scopus subject areas
- Cancer Research
- Molecular Biology
- Oncology
Cite this
Fatty acyl-CoAs inhibit retinoic acid-induced apoptosis in Hep3B cells. / Wan, Yu-Jui Yvonne; Cai, Yan; Cowan, Catherine; Magee, Thomas R.
In: Cancer Letters, Vol. 154, No. 1, 01.06.2000, p. 19-27.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Fatty acyl-CoAs inhibit retinoic acid-induced apoptosis in Hep3B cells
AU - Wan, Yu-Jui Yvonne
AU - Cai, Yan
AU - Cowan, Catherine
AU - Magee, Thomas R.
PY - 2000/6/1
Y1 - 2000/6/1
N2 - Retinoic acid (RA) induces apoptosis in Hep3B human hepatoma cells. 9-Cis-RA (c-RA) had a similar effect as all-trans-RA (t-RA) in inducing cell death in Hep3B cells. RA-induced Hep3B-cell death was associated with inhibited expression of the hepatocyte nuclear factor 4 (HNF-4) gene. Palmitoyl-CoA ((C16:0)-CoA), the reported HNF-4 ligand, prevented RA-induced apoptosis. The effect of (C16:0)-CoA was specific, since palmitic acid and co-enzyme A had no effect in preventing RA-induced apoptosis. Bovine serum albumin (BSA) also prevented RA-induced apoptosis. However, in contrast to BSA, which induced cell growth, (C16:0)-CoA alone had no effect on cell growth. Investigating the possible role of HNF-4 in apoptosis, the reported HNF-4 antagonist (C18:0)-CoA was employed, and it also prevented RA-induced apoptosis. By transient transfection, overexpression of HNF-4 did not prevent RA-induced apoptosis. The induction and prevention of apoptosis caused by RA and (C16:0)-CoA were associated, respectively with the induction and inhibition of the expression of transforming growth factor β (TGFβ), which is known to play a role in apoptosis. Furthermore, RA and (C16:0)-CoA can regulate AP-1, which is a key regulator of the TGFβ gene. Our data indicate that fatty acyl-CoAs can prevent RA-induced apoptosis and that TGFβ, rather than HNF-4, may play a role in these regulatory processes. Our data also suggest that (C16:0)-CoA and (C18:0)-CoA are not the agonist and antagonist for HNF4, respectively in the Hep3B cell system. Copyright (C) 2000 Elsevier Science Ireland Ltd.
AB - Retinoic acid (RA) induces apoptosis in Hep3B human hepatoma cells. 9-Cis-RA (c-RA) had a similar effect as all-trans-RA (t-RA) in inducing cell death in Hep3B cells. RA-induced Hep3B-cell death was associated with inhibited expression of the hepatocyte nuclear factor 4 (HNF-4) gene. Palmitoyl-CoA ((C16:0)-CoA), the reported HNF-4 ligand, prevented RA-induced apoptosis. The effect of (C16:0)-CoA was specific, since palmitic acid and co-enzyme A had no effect in preventing RA-induced apoptosis. Bovine serum albumin (BSA) also prevented RA-induced apoptosis. However, in contrast to BSA, which induced cell growth, (C16:0)-CoA alone had no effect on cell growth. Investigating the possible role of HNF-4 in apoptosis, the reported HNF-4 antagonist (C18:0)-CoA was employed, and it also prevented RA-induced apoptosis. By transient transfection, overexpression of HNF-4 did not prevent RA-induced apoptosis. The induction and prevention of apoptosis caused by RA and (C16:0)-CoA were associated, respectively with the induction and inhibition of the expression of transforming growth factor β (TGFβ), which is known to play a role in apoptosis. Furthermore, RA and (C16:0)-CoA can regulate AP-1, which is a key regulator of the TGFβ gene. Our data indicate that fatty acyl-CoAs can prevent RA-induced apoptosis and that TGFβ, rather than HNF-4, may play a role in these regulatory processes. Our data also suggest that (C16:0)-CoA and (C18:0)-CoA are not the agonist and antagonist for HNF4, respectively in the Hep3B cell system. Copyright (C) 2000 Elsevier Science Ireland Ltd.
KW - Apoptosis
KW - Fatty acyl-CoA
KW - Hepatocyte nuclear factor 4
KW - Hepatoma
KW - Retinoic acid
KW - Transforming growth factor β
UR - http://www.scopus.com/inward/record.url?scp=0034213689&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034213689&partnerID=8YFLogxK
U2 - 10.1016/S0304-3835(00)00341-4
DO - 10.1016/S0304-3835(00)00341-4
M3 - Article
VL - 154
SP - 19
EP - 27
JO - Cancer Letters
JF - Cancer Letters
SN - 0304-3835
IS - 1
ER -