Authors

Yong Zhang*, Yong Wei*, Bing Han**, Yinsheng Wang***, Juehua Jing*, Jun Li*,#

Departments

*Department of Orthopaedics, The Second Hospital of Anhui Medical University, 678 Furong Avenue, Hefei 230601, Anhui, PR China - **Department of Orthopaedics, The First People’s Hospital of Anqing, 42 Xiaosu Avenue, Anqing 246000, Anhui, PR China - ***Department of Orthopaedics, People's Hospital of Yi'an District, 39 Renmin North Road, Tongling 244100, Anhui, PR China

Abstract

Objective: To investigate the inhibitory effect and mechanism of cucurbitacin I on the growth of hepatocellular carcinoma cells. 

Methods: HepG2, QGY-7703 and SMMC-7721 human hepatocellular carcinoma cells were cultured in DMEM cell culture medium under suitable conditions. HepG2, QGY-7703 and SMMC-7721 human hepatocellular carcinoma cells were cultured with cucurbitacin I at different concentrations (1.5 mol/L, 5.5 mol/L and 10 mol/L) for 12 and 36 hours respectively. The activity of HepG2, QGY-7703 and SMMC-7721 cells was detected by CCK-8 method. HepG2 human hepatocellular carcinoma cells were treated and cultured in cucurbitacin I medium containing different concentrations (1.5 mol/L, 5.5 mol/L, 10 mol/L). After Hoechst 33343 staining, the cloning formation of HepG2 cells was observed by clone formation assay. Flow cytometry was used to detect the apoptosis of HepG2 cells. Detection of anti-apoptotic factors by Western blot. 

Results: Compared with the control group, the activity of HepG2, QGY-7703 and SMMC-7721 cells cultured with cucurbitacin I at different concentrations (1.5 mol/L, 5.5 mol/L and 10 mol/L) decreased significantly after 12 and 36 hours (P<0.05). Compared with the control group, the cloning rate of HepG2 cells treated with cucurbitacin I at different concentrations (1.5 mol/L, 5.5 mol/L and 10 mol/L) was significantly lower (P<0.05). Compared with the control group, HepG2 cells were treated with cucurbitacin I at different concentrations (1.5 mol/L, 5.5 mol/L, 10 mol/L). With the increase of cucurbitacin I concentration, there were chromatin shrinkage and cell nucleolysis in HepG2 cells, which aggravated cell apoptosis. The levels of anti-apoptotic factors Mcl-1, survivin, p-STAT3 (Y705) and STAT3 in HepG2 cells treated with cucurbitacin I at different concentrations (1.5 mol/L, 5.5 mol/L and 10 mol/L) were significantly decreased. 

Conclusion: Cucurbitacin I can aggravate apoptosis by reducing the level of anti-apoptotic factors, thus inhibiting the growth of hepatocellular carcinoma cells.

Keywords

Cucurbitacin I, hepatocellular carcinoma cells, inhibition.

DOI:

10.19193/0393-6384_2019_6_506