Acts as an electrogenic sodium (Na(+)) and chloride (Cl-)-dependent sodium-coupled solute transporter, including transport of monocarboxylates (short-chain fatty acids including L-lactate, D-lactate, pyruvate, acetate, propionate, valerate and butyrate), mocarboxylate drugs (nicotinate, benzoate, salicylate and 5-aminosalicylate) and ketone bodies (beta-D-hydroxybutyrate, acetoacetate and alpha-ketoisocaproate), with a Na(+):substrate stoichiometry of between 4:1 and 2:1 (    ). Catalyzes passive carrier mediated diffusion of iodide . Mediates iodide transport from the thyrocyte into the colloid lumen through the apical membrane . May be responsible for the absorption of D-lactate and monocarboxylate drugs from the intestinal tract . Acts as a tumor suppressor, suppressing colony formation in colon cancer, prostate cancer and glioma cell lines ( ). May play a critical role in the entry of L-lactate and ketone bodies into neurons by a process driven by an electrochemical Na(+) gradient and hence contribute to the maintenance of the energy status and function of neurons . Mediates sodium-coupled electrogenic transport of pyroglutamate (5-oxo-L-proline) . Can mediate the transport of chloride, bromide, iodide and nitrate ions when the external concentration of sodium ions is reduced .
Subcellular locations: Apical cell membrane
Expressed at the apical membrane of normal tall thyrocytes and of colonic epithelial cells.
Expressed in normal thyroid, localized at the apical pole of thyroid cells facing the colloid lumen, but expression profoundly decreased in thyroid carcinomas. Expressed in normal colon but absent in colon aberrant crypt foci and colon cancers. Present in normal kidney cortex, brain, prostate, gastric mucosa and breast tissue but was significantly down-regulated in primary gliomas, gastric cancer, prostate tumors and breast tumors.