Cytosolic Sulfotransferase Activity in Cancer Biology

Cytosolic sulfotransferases (SULTs) are a family of phase II enzymes that catalyse the transfer of a sulphate group from 3′-phosphoadenosine 5′-phosphosulphate (PAPS) to a wide range of endogenous compounds, xenobiotics and procarcinogens. Through sulphation, these enzymes modulate the biological activities, receptor affinities and elimination pathways of hormones, neurotransmitters and environmental chemicals. In cancer biology, altered expression or polymorphic variants of SULT isoforms can influence tumour initiation, progression and response to therapy by changing the balance between detoxification and bioactivation of carcinogenic substrates. Overexpression of specific SULTs in tumour cells may drive proliferation by inactivating growth‐regulating hormones or by promoting the elimination of drug metabolites, while loss‐of‐function variants can increase individual susceptibility to chemical carcinogens. Emerging evidence also highlights SULTs as candidate biomarkers for prognosis and as targets for small‐molecule inhibitors designed to enhance chemopreventive strategies. Understanding the structural basis of substrate selectivity, the impact of genetic variants and the development of selective assays has thus become central to exploiting cytosolic sulfotransferase activity in oncology.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Cytosolic Sulfotransferase Activity in Cancer Biology publication trend

The graph below shows the total number of articles in cytosolic sulfotransferase activity in cancer biology across all publications each year (not limited to Nature Index journals).

Technical terms

Cytosolic sulfotransferase (SULT): An enzyme that transfers a sulphate group from PAPS to substrates in the cytosol, affecting solubility and activity.

3′-Phosphoadenosine 5′-phosphosulphate (PAPS): The universal sulphate donor molecule used by sulfotransferases in sulphonation reactions.

Isoform: A distinct form of a protein arising from the same gene but differing in amino-acid sequence or expression context.

Polymorphism: A genetic variation at a specific locus that may alter protein function or expression.

Procarcinogen: A compound that requires metabolic activation, such as sulphation, to become a carcinogen.

Apoptosis: Programmed cell death, a regulated process by which cells self-destruct in response to stress or damage.

References

1. A Novel Fluorescence-Based Microplate Assay for High-Throughput Screening of hSULT1As Inhibitors. Biosensors (2024).
2. Structural and Dynamic Characterizations Highlight the Deleterious Role of SULT1A1 R213H Polymorphism in Substrate Binding. International Journal of Molecular Sciences (2019).
3. Hydroxysteroid Sulfotransferase SULT2B1b Promotes Hepatocellular Carcinoma Cells Proliferation In Vitro and In Vivo. PLOS ONE (2013).