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Page 8 of 18 Kouroumalis et al. Hepatoma Res 2018;4:34 I http://dx.doi.org/10.20517/2394-5079.2018.33

Figure 1. Anti-tumoral effect of somatostatin is achieved through various cellular pathways leading to inhibition of cell proliferation,
inflammation, fibrosis and angiogenesis. Apoptosis is increased. It seems that a reduction of tumor associated macrophages (TAM) and
a swift from M2 polarization in Kupffer cells may also help in the final effect

significantly prolonged the survival of rabbits with experimental liver cancer previously treated with tumor
arterial embolization (TAE) . Treatment with octreotide and celecoxib after TAE, synergistically inhibits
[101]
hepatic allograft metastasis by promoting tumor encapsulation and inhibition of angiogenesis .
[102]
Lanreotide, a long acting SSA, was used as a cancer chemopreventive agent in a series of animal experiments.
Thus, lanreotide was able to decrease the size of diethyl- nitrosamine induced liver preneoplastic foci by
inhibiting cell proliferation and increasing apoptosis. This was associated with a decrease of cyclin D1 and
an increase of p27kip1 . Lanreotide also reduced the number of chemically induced HCCs and significantly
[103]
decreased fibrosis and the level of angiogenic factors [104,105] . In another animal model, albino mice developed
HCC by injection with diethyl-nitrosamine. The administration of octreotide alone or in combination with
a plant extract prevented malignant transformation. This effect was associated with a substantial reduction
of oxidative stress observed in the control animals .
[106]
A rather intriguing finding was recently reported in rats with a high fat diet induced obesity. Octreotide
increased hepatic glucogenesis associated with increased glucose synthase and decreased fasting blood