| Objective: To observe the inhibition of sorafenib combined withoctreotide on human hepatoma cell line HepG2in vitro and to explore itsmechanism.Methods: HepG2cells were treated with gradient of differentconcentrations of a separate and combined effects of sorafenib andoctreotide with the untreated cells used for control. The cell killing effect ofthe treatment was determined by CCK-8kit, and the rate of the cell apoptosiswas detected by flow cytometry. Fluoresence microscope was used forobserving the cell growth. Elisa was used for detecting the VEGF. Westernblot was performed to determine the expressions of Mcl-1, ERK1/2andp-ERK1/2in the cells.Result: Sorafenib and octreotide used separately and combinedly bothinhibited the proliferation and inducted apoptosis of HepG2cells. Theefficiency of the combined group was higher than other groups (P<0.05).The fluorescence microscopy showed the combination group and individualtreatment group appeared phosphatidylserine (PS), which is the marker ofearly apoptosis,but not appeared in the control group. The VEGF of combination group was lower than alone treatment group and control group(F=1019.725， P<0.05). Western blotting showed Mcl-1expression ofoctreotide group had no difference from the control group (P>0.05), but thecombined group was significantly lower than the single treatment group andcontrol group (P<0.05).The expression of ERK1/2in every group has nodifference (P>0.05). Also, Western blotting showed p-ERK1/2expression ofevery sample group was lower to the control group (F=2.401, P<0.05), thecombined group was lower than the single treatment group (P<0.05)。Conclusions Sorafenib and octreotide can inhibit the proliferation andinduce the apoptosis of human hepatoma cell line HepG2.The combinedeffect is more significant (P <0.05), which showed synergistic effects,. Themechanism of this phenomenon may depend on synergistic inhibition of theVEGF, decreasing of anti-apoptotic protein Mcl-1and proliferation ofp-ERK1/2. |
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