Cell migration plays a critical role in the formation of tumor metastases. On a cellular level, the intracellular Ca2+ concentration is a key regulator of various parts of the cellular migration machi-nery. However, the molecular identity of the Ca2+ channels regulating the intracellular Ca2+ homeostasis of migrating cells is still unknown. It was shown that TRPV1 channels modulate Ca2+ entry into HepG2 hepatoblastoma cells. This effect was more pronounced in migrating HepG2 cells treated with hepatocyte growth factor (HGF). We therefore set out to study the role of TRPV1 channels in migration of HepG2 cells. Migration was monitored with time lapse video microscopy in the presence or absence of HGF. The speed of HGF-treated cells is 0.160.02 mm/min, and cells cover 19.12.5 mm within 5 h. The TRPV1 channel activator capsaicin stimulates migration. This effect is more pronounced in HGF-treated cells. Patch clamp experiments reveal a capsaicin-activated current only in HGF-treated HepG2 cells. As shown in Western blots, TRPV1 expression does not change upon HGF treatment. Pretreatment with the TRPV1 blocker capsazepine completely reversed the effect of capsaicin on migration. We conclude that TRPV1 channels are part of the cellular migration machiney of HepG2 cells.