Target intelligence / Profile preview

Mitochondrial coenzyme A transporter SLC25A42 (SLC25A42)

Target
SLC25A42
Molecular classification
Transporter, Solute carrier family (SLC25), Mitochondrial inner membrane carrier protein
01

Overview

SLC25A42 (Mitochondrial coenzyme A transporter SLC25A42) is a member of the solute carrier family 25, residing in the inner mitochondrial membrane. It catalyzes the exchange of coenzyme A (CoA) from the cytosol into the mitochondrial matrix, in exchange for (deoxy)adenine nucleotides and adenosine 3',5'-diphosphate, thus supporting mitochondrial metabolic processes involved in fatty acid oxidation, energy production, and other biosynthetic reactions[2][6]. This transporter has been shown to play a crucial role in regulating cell metabolism and mitochondrial energy status. Notably, in cancer—particularly gastric cancer—SLC25A42 is upregulated, promotes tumor cell proliferation, and enables cancer cells to resist ferroptosis (a lipid peroxidation-driven form of cell death) by sustaining fatty acid oxidation and mitochondrial function[4]. Its expression correlates with poor prognosis in gastric cancer patients, making it a potential oncogenic factor and an investigational therapeutic target in oncology[4].

Other names
MGC26694Mitochondrial coenzyme A transporterSolute carrier family 25 member 42MECREN
02

Mechanism of action

Experimental inhibition or knockdown of SLC25A42 increases cellular susceptibility to ferroptosis, which can be rescued by ferroptosis inhibitors such as Fer-1, suggesting modulation of SLC25A42 can alter cell sensitivity to this programmed cell death pathway[4].

03

Biological functions

Mitochondrial transport of coenzyme A (CoA)Exchange of CoA for (deoxy)adenine nucleotidesRegulation of mitochondrial metabolismLipid metabolism reprogrammingRegulation of fatty acid oxidationInhibition of ferroptosis (a form of regulated cell death)Promotion of cell proliferation (notably in gastric cancer cells)
04

Disease associations

Cancer (specifically gastric cancer, where it is upregulated and promotes tumor growth)Potential involvement in metabolic diseases or mitochondrial dysfunction (based on its metabolic role)
05

Safety considerations

Targeting SLC25A42 could disrupt mitochondrial function and energy metabolism in non-malignant tissues due to its essential role in CoA import, raising concerns about on-target toxicity[2][6]
06

Interacting drugs

No clinically approved drugs are currently known to specifically target SLC25A42

1 more in the full profile.

07

Biomarkers

Overexpression of SLC25A42 is associated with poor prognosis in gastric cancer and thus may serve as a prognostic biomarker[4]Increased SLC25A42 expression in tumor tissue (biomarker for aggressive cancer phenotype)[4]

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