Title : Targeting INMT and interrupting its methylation pathway for the treatment of castration resistant prostate cancer.

Pub. Date : 2021 Sep 29

PMID : 34587977






2 Functional Relationships(s)
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1 Gene knockdown/overexpression, MTT and mouse cancer models were used to examine the role of INMT as well as the anticancer efficacy of INMT inhibitor N,N-dimethyltryptamine (DMT), the SMYD3 inhibitor BCl-12, the selenium compounds methaneseleninic acid (MSA) and Se-(Methyl)selenocysteine hydrochloride (MSC), and the newly identified endogenous INMT substrate Bis(7)-tacrine. 1,7-N-heptylene-bis-9,9'-amino-1,2,3,4-tetrahydroacridine indolethylamine N-methyltransferase Mus musculus
2 Importantly, INMT knockdown significantly increased the anticancer effect of the exogenous selenium compounds methaneseleninic acid (MSA) and Se-(Methyl)selenocysteine hydrochloride (MSC) as well as the endogenous metabolite Bis(7)-tacrine. 1,7-N-heptylene-bis-9,9'-amino-1,2,3,4-tetrahydroacridine indolethylamine N-methyltransferase Mus musculus