Target intelligence / Profile preview

Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3C (APOBEC3C)

Target
APOBEC3C
Molecular classification
Enzyme, Cytidine deaminase, Nucleic acid editing enzyme
01

Overview

Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3C (APOBEC3C) is a cytidine deaminase and member of the APOBEC3 family, functioning primarily in innate antiviral immunity. It edits single-stranded DNA by catalyzing the deamination of cytidine to uridine, an activity that restricts the replication of endogenous retroelements and various retroviruses, though it inhibits HIV-1 only weakly but is more effective against simian immunodeficiency virus[1][3][4][5]. APOBEC3C is highly expressed in response to genotoxic stress, regulated by p53, and is mainly localized to the nucleolus, where it is excluded from DNA damage sites[5]. In cancer, especially prostate cancer, APOBEC3C acts as a potential tumor suppressor—its downregulation is associated with cancer progression, adverse outcomes, and resistance to androgen receptor antagonists, making it a clinically relevant biomarker. No current small-molecule drugs directly target its activity, but its modulation has implications for antiviral defense, cancer biology, and therapeutic resistance[2][4][5][7].

Other names
DNA dC->dU-editing enzyme APOBEC-3CAPOBEC1LPBIA3CARDC2ARDC4ARP5APOBEC1-likePhorbolin IbK150C2.3Probable DNA dC->dU-editing enzyme APOBEC-3CApolipoprotein B editing enzyme catalytic polypeptide-like 3C
02

Mechanism of action

Not applicable for direct drugs, but resistance to AR pathway inhibitors in prostate cancer when APOBEC3C expression is low[2]

03

Biological functions

Innate immune responseRestriction of retroviral infectionRestriction of endogenous retroelement integrationDNA mutation (cytidine to uridine editing in single-stranded DNA)RNA-editing (to a limited degree)
04

Disease associations

CancerInfection (notably retroviruses: HIV-1, SIV, and others)Potential role in therapy resistance (e.g., resistance to AR antagonists in prostate cancer)
05

Safety considerations

Potential for off-target mutagenesis and genome instability if pharmacologically modulated[4][5]No current safety data for direct targeting in humans
06

Interacting drugs

Abiraterone (resistance marker in prostate cancer)[2]

2 more in the full profile.

07

Biomarkers

Prognostic biomarker in prostate cancer (low APOBEC3C expression correlates with poor prognosis, resistance to AR antagonists, and higher stages/relapse rates)[2]

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