Enhanced SLC35B2/SAV1 Sulfation Axis Promotes Tumor Growth through Inhibiting Hippo Signaling in Hepatocellular Carcinoma

By mass spectrometry and bioinformatics analysis, investigators identified SAV1 as a novel substrate of PTS in HCC. Oxidative stress upregulates the transcription of SLC35B2, a Golgi-resident transporter of sulfate donor 3’-phosphoadenosine 5’-phosphosulfate, leading to increased sulfation of SAV1.