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A selective aryl hydrocarbon receptor modulator 3,3'-Diindolylmethane inhibits gastric cancer cell growth.

Yin XF, Chen J, Mao W, Wang YH, Chen MH - J. Exp. Clin. Cancer Res. (2012)

Bottom Line: Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor associated with gastric carcinogenesis. 3,3'-Diindolylmethane (DIM) is a relatively non-toxic selective AhR modulator.Flow cytometry analysis showed that DIM arrested cell cycle in G1 phase and induced cell apoptosis.Selective aryl hydrocarbon receptor modulator 3,3'-Diindolylmethane inhibits SGC7901 cell proliferation by inducing apoptosis and delaying cell cycle progression.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Gastroenterology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.

ABSTRACT

Background: Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor associated with gastric carcinogenesis. 3,3'-Diindolylmethane (DIM) is a relatively non-toxic selective AhR modulator. This study was to detect the effects of DIM on gastric cancer cell growth.

Methods: Gastric cancer cell SGC7901 was treated with DIM at different concentrations (0,10,20,30,40,50 μmol/L) with or without an AhR antagonist, resveratrol. The expression of AhR and Cytochrome P4501A1 (CYP1A1), a classic target gene of AhR pathway, were detected by RT-PCR and Western blot; cell viability was measured by MTT assay, and the changes in cell cycle and apoptosis were analyzed by flow cytometry.

Results: RT-PCR and western-blot showed that with the increase of the concentration of DIM, AhR protein gradually decreased and CYP1A1 expression increased, suggesting that DIM activated the AhR pathway and caused the translocation of AhR from cytoplasm to nucleus. MTT assay indicated that the viability of SGC7901 cells was significantly decreased in a concentration- and time-dependent manner after DIM treatment and this could be partially reversed by resveratrol. Flow cytometry analysis showed that DIM arrested cell cycle in G1 phase and induced cell apoptosis.

Conclusion: Selective aryl hydrocarbon receptor modulator 3,3'-Diindolylmethane inhibits SGC7901 cell proliferation by inducing apoptosis and delaying cell cycle progression. AhR may be a potential therapeutic target for gastric cancer treatment.

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Viability of SGC7901 cells after DIM treatment was assessed by MTT assay. Viability of SGC7901 cells was significantly decreased in a concentration- and time-dependent manner after DIM treatment. Resveratrol(10 μmol/L) could partially reverse the inhibition effects of DIM(30 μmol/L) on cellur proliferation.
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Figure 3: Viability of SGC7901 cells after DIM treatment was assessed by MTT assay. Viability of SGC7901 cells was significantly decreased in a concentration- and time-dependent manner after DIM treatment. Resveratrol(10 μmol/L) could partially reverse the inhibition effects of DIM(30 μmol/L) on cellur proliferation.

Mentions: Proliferation of SGC7901 cells was determined by MTT assay after 6–72 h of treatment with increasing concentrations of DIM (0–50 μmol/L). Results showed that DIM inhibited SGC7901 cellular proliferation in a concentration- and time-dependent manner, Resveratrol (10 μmol/L) could partially reverse the inhibition effects of DIM (30 μmol/L) on cellur proliferation at the time points: 6 h and 12 h (Figure 3), but we did not find the reversal effects at other time points (24 h, 48 h and 72 h, data were not shown).


A selective aryl hydrocarbon receptor modulator 3,3'-Diindolylmethane inhibits gastric cancer cell growth.

Yin XF, Chen J, Mao W, Wang YH, Chen MH - J. Exp. Clin. Cancer Res. (2012)

Viability of SGC7901 cells after DIM treatment was assessed by MTT assay. Viability of SGC7901 cells was significantly decreased in a concentration- and time-dependent manner after DIM treatment. Resveratrol(10 μmol/L) could partially reverse the inhibition effects of DIM(30 μmol/L) on cellur proliferation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3403951&req=5

Figure 3: Viability of SGC7901 cells after DIM treatment was assessed by MTT assay. Viability of SGC7901 cells was significantly decreased in a concentration- and time-dependent manner after DIM treatment. Resveratrol(10 μmol/L) could partially reverse the inhibition effects of DIM(30 μmol/L) on cellur proliferation.
Mentions: Proliferation of SGC7901 cells was determined by MTT assay after 6–72 h of treatment with increasing concentrations of DIM (0–50 μmol/L). Results showed that DIM inhibited SGC7901 cellular proliferation in a concentration- and time-dependent manner, Resveratrol (10 μmol/L) could partially reverse the inhibition effects of DIM (30 μmol/L) on cellur proliferation at the time points: 6 h and 12 h (Figure 3), but we did not find the reversal effects at other time points (24 h, 48 h and 72 h, data were not shown).

Bottom Line: Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor associated with gastric carcinogenesis. 3,3'-Diindolylmethane (DIM) is a relatively non-toxic selective AhR modulator.Flow cytometry analysis showed that DIM arrested cell cycle in G1 phase and induced cell apoptosis.Selective aryl hydrocarbon receptor modulator 3,3'-Diindolylmethane inhibits SGC7901 cell proliferation by inducing apoptosis and delaying cell cycle progression.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Gastroenterology, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, People's Republic of China.

ABSTRACT

Background: Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor associated with gastric carcinogenesis. 3,3'-Diindolylmethane (DIM) is a relatively non-toxic selective AhR modulator. This study was to detect the effects of DIM on gastric cancer cell growth.

Methods: Gastric cancer cell SGC7901 was treated with DIM at different concentrations (0,10,20,30,40,50 μmol/L) with or without an AhR antagonist, resveratrol. The expression of AhR and Cytochrome P4501A1 (CYP1A1), a classic target gene of AhR pathway, were detected by RT-PCR and Western blot; cell viability was measured by MTT assay, and the changes in cell cycle and apoptosis were analyzed by flow cytometry.

Results: RT-PCR and western-blot showed that with the increase of the concentration of DIM, AhR protein gradually decreased and CYP1A1 expression increased, suggesting that DIM activated the AhR pathway and caused the translocation of AhR from cytoplasm to nucleus. MTT assay indicated that the viability of SGC7901 cells was significantly decreased in a concentration- and time-dependent manner after DIM treatment and this could be partially reversed by resveratrol. Flow cytometry analysis showed that DIM arrested cell cycle in G1 phase and induced cell apoptosis.

Conclusion: Selective aryl hydrocarbon receptor modulator 3,3'-Diindolylmethane inhibits SGC7901 cell proliferation by inducing apoptosis and delaying cell cycle progression. AhR may be a potential therapeutic target for gastric cancer treatment.

Show MeSH
Related in: MedlinePlus