3,3′-Diindolylmethane ameliorates experimental hepatic fibrosis via inhibiting miR-21 expression

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Smad3-Mediated Upregulation of miR-21 Promotes Renal Fibrosis

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3,3′-Diindolylmethane inhibits breast cancer cell growth via miR-21-mediated Cdc25A degradation

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3,3′-Diindolylmethane attenuates experimental arthritis and osteoclastogenesis

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Toxic and Chemopreventive Ligands Preferentially Activate Distinct Aryl Hydrocarbon Receptor Pathways: Implications for Cancer Prevention

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3,3'-Diindolylmethane Enhances Taxotere-Induced Apoptosis in Hormone-Refractory Prostate Cancer Cells through Survivin Down-regulation

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Alteration of microRNA expression in vinyl carbamate-induced mouse lung tumors and modulation by the chemopreventive agent indole-3-carbinol

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A class of imidazolium salts is anti-oxidative and anti-fibrotic in hepatic stellate cells

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Modulation of Hepatic Fibrosis by c-Jun-N-Terminal Kinase Inhibition

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3,3′-diindolylmethane attenuates colonic inflammation and tumorigenesis in mice

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Association of MicroRNA Expression in Hepatocellular Carcinomas with Hepatitis Infection, Cirrhosis, and Patient Survival

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(2008) Scott L. Friedman   GASTROENTEROLOGY

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miR-21 Gene Expression Triggered by AP-1 Is Sustained through a Double-Negative Feedback Mechanism

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MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts

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An autoregulatory loop mediated by miR-21 and PDCD4 controls the AP-1 activity in RAS transformation

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