Parathyroid hormone (1–34) [PTH‐(1–34)] has been shown to stimulate sodium‐dependent phosphate transport (NaPiT) in UMR‐106 osteoblast‐like cells through a cAMP‐dependent mechanism. Whether a synthetic amino‐terminal fragment of parathyroid hormone‐related protein (PTHrP) or the full‐length molecule, which are recognized to interact with the same receptor as PTH, affect NaPiT in the same way is not known. We investigated and compared the effects of bPTH‐(1–34), PTHrP‐(1–34), and PTHrP‐(1–141) on NaPiT and cAMP production in the osteoblastic cell line UMR‐106. Each of the three peptides increased cAMP production and exerted a concentration‐dependent stimulation of NaPiT after incubation for 4–6 h. We also studied the effect of transforming growth factor‐α (TGF‐α), which is another tumoral product secreted by certain hypercalcemia‐associated tumors, on NaPiT and the TGF‐α‐induced modulation of the response to PTHrP or PTH. TGF‐α caused a 30% stimulation of NaPiT, which remained stable from 6 to 24 h, by a cAMP‐independent mechanism. In contrast, TGF‐α attenuated cAMP production stimulated by PTH, PTHrP‐(1–34), or PTHrP‐(1–141). PTHrP or PTH did not further increase NaPiT in TGF‐α‐treated cells. These results indicate that NaPiT, a possibly important function of osteoblastic cells, was similarly affected by PTH and PTHrP. TGF‐α increased NaPiT and modulated in a similar way the effects of both PTH and PTHrP.