Fatty acyl-CoAs inhibit retinoic acid-induced apoptosis in Hep3B cells

Yu-Jui Yvonne Wan, Yan Cai, Catherine Cowan, Thomas R. Magee

Research output: Contribution to journalArticle

15 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)19-27
Number of pages9
JournalCancer Letters
Volume154
Issue number1
DOIs
StatePublished - Jun 1 2000

Fingerprint

Tretinoin
Hepatocyte Nuclear Factor 4
Coenzyme A
Apoptosis
Transforming Growth Factors
Bovine Serum Albumin
Cell Death
Palmitoyl Coenzyme A
Palmitic Acid
Transcription Factor AP-1
Growth
Genes
Transfection
Hepatocellular Carcinoma
Ligands

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 journalArticle

Wan, Yu-Jui Yvonne ; Cai, Yan ; Cowan, Catherine ; Magee, Thomas R. / Fatty acyl-CoAs inhibit retinoic acid-induced apoptosis in Hep3B cells. In: Cancer Letters. 2000 ; Vol. 154, No. 1. pp. 19-27.
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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.",
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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.

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