Phytochemical Name : 3,3'-diindolylmethane (DIM)

Properties Information
PhytoCAT-ID PhytoCAT-1063
Phytochemical name or plant extracts 3,3'-diindolylmethane (DIM)
PMID 21154750
Literature evidence Because elevated expression of FoxM1 has been observed in human breast cancers, FoxM1 has attracted much attention in recent years as a potential target for the prevention and/or therapeutic intervention in breast cancer.
IUPAC name 3-(1H-indol-3-ylmethyl)-1H-indole
Phytochemicals’ class or type of plant extracts Indole
Source of phytochemicals or plant Extracts Arundo donax
Geographical availability Afghanistan, Assam, Bangladesh, Cambodia, China South-Central, China Southeast, Cyprus, East Himalaya, Gulf States, Hainan, India, Iran, Iraq, Japan, Kazakhstan, Laos, Lebanon-Syria, Myanmar, Nansei-shoto, Nepal, Ogasawara-shoto, Oman, Pakistan, Palestine, Sinai, Tadzhikistan, Thailand, Tibet, Transcaucasus, Turkey, Turkmenistan, Uzbekistan, Vietnam, West Himalaya, Yemen
Plant parts NA
Other cancers Breast cancer, Ovarian cancer, Prostate cancer
Target gene or protein FoxM1, CXCR4, CXCL12, p21, Cadherin-11, Plasminogen
Gene or Protein evidence We also found that knock down of FoxM1 expression by small interfering RNA (siRNA) transfection increased DIM-induced cell growth inhibition, whereas over-expression of FoxM1 by cDNA transfection attenuated DIM-induced cell growth inhibition, suggesting the mechanistic role of FoxM1. CXCR4 and CXCL12 down-regulation: a novel mechanism for the chemoprotection of 3,3'-diindolylmethane for breast and ovarian cancers. 3,3'-diindolylmethane induced a G(1) cell cycle arrest in human breast cancer MCF-7 cells by a mechanism that included increased expression of p21. DIM and curcumin decreased cadherin-11 and increased urokinase-type plasminogen activator levels correlated with increased cell motility.
Target pathways DIM can inactivate Akt/ Nuclear factor-κB (NF-κB) signaling and induce apoptosis in cancer cells.
IC50 NA
Potency We conclude that inactivation of FoxM1 and its target genes by DIM could enhance the therapeutic efficacy of Taxotere in breast cancer, which could be a useful strategy for the prevention and/or treatment of breast cancer.
Cell line/ mice model MDA-MB-231, MCF-7, MDA-MB-468, SKBR-3, BALB/c mice, T47D, Saos2
Additional information  The results suggest that interactions of DIM, and/or its mono-hydroxy metabolites, with CYP2B1 and CYP2B2 found to occur in hepatic microsomes upon addition of DIM or co-treatment of rats with DIM affect the rates of relevant oxidations of E2, and potentially protect against estrogen-dependent tumorigenesis. In addition, antioxidants significantly attenuated 3,3'-diindolylmethane-induced activation of p38 and JNK and induction of p21, indicating that oxidative stress is the major trigger of these events. The addition of other AhR ligands, alpha-naphthoflavone (alpha-NF, 10 microM) and luteolin (10 microM), to the culture media resulted in a similar suppression in ER-alpha mRNA levels to that caused by 5 microM DIM.
PubChem ID 3071
Additional PMIDs 15623462 30301388 34066056 18025290 18486294 19064917 25048790 15665315 16651444 19056653 19223575 21154750 21767081 25613194 10449193 12738179 16488130 19864400 10652612 8912651 11931841 11849035 16544949 18378071 23968581 32710170 23140282 26249585
Additional sources of information https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:390837-1
Safety NA