Oleocanthal inhibits growth and metastasis by blocking activation of STAT3 in human hepatocellular carcinoma

In the present study was explored by Pei et al., the anti-cancer capacity of oleocanthal in human hepatocellular carcinoma (HCC). Oleocanthal inhibited proliferation and cell cycle progression and induced apoptosis in HCC cells in vitro and suppressed tumor growth in an orthotopic HCC model. Oleocanthal also inhibited HCC cell migration and invasion in vitro and impeded HCC metastasis in an in vivo lung metastasis model. Oleocanthal acted by inhibiting epithelial-mesenchymal transition (EMT) through downregulation Twist, a protein which is a direct target of the transcription factor STAT3.

Oleocanthal also reduced STAT3 nuclear translocation and DNA binding activity, ultimately downregulating its downstream effectors, including the cell cycle protein Cyclin D1, the anti-apoptotic proteins Bcl-2 and survivin, and the invasion-related protein MMP2. Overexpression of constitutively active STAT3 partly reversed the anticancer effects of oleocanthal, which inhibited STAT3 activation by decreasing the activities of JAK1 and JAK2 and increasing the activity of SHP-1. These data suggest that oleocanthal may be a promising candidate for HCC treatment.

Oleocanthal has strong anti-tumor properties in human liver cells, as it reduces tumor cell proliferation, inhibits tumor growth and simultaneously causes the death of many cancer cells.

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