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The lycopene metabolite acycloretinoic acid is a weak activator of RARs
Quote from
tim on September 2, 2020, 6:24 am
Among identified lycopene metabolites, acycloretinoic acid has been shown to inhibit cell proliferation (82–84), induce apoptosis (85), and enhance gap junction communication (86). As an analog of retinoic acid, the ability of acycloretinoic acid to activate RAR was first examined by Ben-Dor et al (83) and Stahl et al (86). Although acycloretinoic acid is able to activate RARE-driven luciferase gene transcription, the required concentration is much higher than that of all-trans retinoic acid, which suggests that acycloretinoic acid is a weak activator of RARs (83, 86). Because of the similarity in chemical structures among apo-10′-lycopenoic acid, acycloretinoic acid, and all-trans retinoic acid (Figure 2), we questioned whether apo-10′-lycopenoic acid is an activator of RARs. We showed that treatment with 3–5 μmol apo-10′-lycopenoic acid/L significantly increased the mRNA level of RARβ, which is a transcriptional target of RARs (87), in lung cells (normal human bronchial epithelial, BEAS-2B, and A549 cells) (57). We then constructed a reporter vector containing the RARβ promoter fragment in the promoter region of luciferase gene. We showed that apo-10′-lycopenoic acid treatment increased the luciferase activity of HeLa cells transfected with this reporter vector. When the RARE in RARβ promoter was mutated, the ability of apo-10′-lycopenoic acid to transactivate RARβ promoter was abolished. These results suggest that apo-10′-lycopenoic acid can transactivate RARs and that activation of RARs may account for the growth inhibitory effect of apo-10′-lycopenoic acid (57).
https://academic.oup.com/ajcn/article/96/5/1214S/4577193
Among identified lycopene metabolites, acycloretinoic acid has been shown to inhibit cell proliferation (82–84), induce apoptosis (85), and enhance gap junction communication (86). As an analog of retinoic acid, the ability of acycloretinoic acid to activate RAR was first examined by Ben-Dor et al (83) and Stahl et al (86). Although acycloretinoic acid is able to activate RARE-driven luciferase gene transcription, the required concentration is much higher than that of all-trans retinoic acid, which suggests that acycloretinoic acid is a weak activator of RARs (83, 86). Because of the similarity in chemical structures among apo-10′-lycopenoic acid, acycloretinoic acid, and all-trans retinoic acid (Figure 2), we questioned whether apo-10′-lycopenoic acid is an activator of RARs. We showed that treatment with 3–5 μmol apo-10′-lycopenoic acid/L significantly increased the mRNA level of RARβ, which is a transcriptional target of RARs (87), in lung cells (normal human bronchial epithelial, BEAS-2B, and A549 cells) (57). We then constructed a reporter vector containing the RARβ promoter fragment in the promoter region of luciferase gene. We showed that apo-10′-lycopenoic acid treatment increased the luciferase activity of HeLa cells transfected with this reporter vector. When the RARE in RARβ promoter was mutated, the ability of apo-10′-lycopenoic acid to transactivate RARβ promoter was abolished. These results suggest that apo-10′-lycopenoic acid can transactivate RARs and that activation of RARs may account for the growth inhibitory effect of apo-10′-lycopenoic acid (57).
https://academic.oup.com/ajcn/article/96/5/1214S/4577193
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