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Yan Y.-Y.,Shanxi Datong University | Guo Y.,Wuhai Municipal Peoples Hospital | Zhang W.,Wuhai Municipal Peoples Hospital | Zhang W.,Inner Mongolia Medical College | And 4 more authors.
Journal of B.U.ON. | Year: 2014

Purpose: To investigate whether celastrol could show synergism combined with lapatinib in HepG2 human hepatocellular carcinoma (HCC) cell line in vitro. Methods: The effects of treatment with lapatinib and/or celastrol on cell growth were determined using MTT assay. Drug synergy was determined using combination index (CI) methods derived from Chou-Talalay equations using CalcuSyn software. Apoptotic morphology was observed by fluorescence microscope with Hoechst 33258 staining. The expression of EGFR of cell surface was performed by flow cytometry. Changes of apoptotic and growth pathways-related proteins were analysed by Western blotting. Results: The combination of celastrol and lapatinib produced strong synergy in growth inhibition and apoptosis in vitro in comparison to single-agent treatments. Moreover, celastrol enhanced the ability of lapatinib to down regulate EGFR protein expression in HepG2 cells. Conclusion: These data indicate that the combination of celastrol and lapatinib could be used as a novel combination regimen which could hopefully provide strong anticancer synergy in the treatment of HCC.


Guo Y.,Wuhai Municipal Peoples Hospital | Zhang W.,Wuhai Municipal Peoples Hospital | Zhang W.,Inner Mongolia Medical College | Yan Y.-Y.,Shanxi Datong University | And 4 more authors.
Journal of B.U.ON. | Year: 2013

Purpose: To investigate the anticancer properties implicated in a natural triterpenoid (pristimerin)-induced apoptosis and inhibited proliferation in human hepatocellular carcinoma (HCC) HepG2 cell line. Methods: The cytotoxic activity of pristimerin in HepG2 cells was determined by MTT assay. Apoptotic morphology was observed by fluorescence microscope with Hoechst 33258 staining and percent apoptosis was measured by annexin V/PI double staining. DiOC6 for mitochondrial potential (Δψm) and DCFH-DA for reactive oxygen species (ROS) were determined by flow cytometry. Changes of apoptotic-related proteins were analysed by Western blot. Results: Pristimerin exerted a potent cytotoxic effect on HepG2 cells. After HepG2 cells were treated with pristimerin, typical apoptotic bodies, increasing the proportion of apoptotic annexin V-positive cells and activation of caspase-3 were detected in a dose-dependent manner. It was intriguing that pristimerin increased the generation of ROS with a collapse of the mitochondrial membrane potential in the cells. In addition, there was significant change in other mitochondrial membrane proteins triggered by pristimerin, such as Bcl-2 and Bax. Pristimerin also effectively induced subsequent release of cytochrome C from mitochondria into the cytosol, downregulated EGFR protein expression and inhibited downstream signaling pathways in HepG2 cells. Pretreatment with N-acetylcysteine (NAC) blocked ROS generation and resulted in loss of mitochondrial membrane potential, release of cytochrome C and apoptosis induced by pristimerin. Conclusion: These data indicate that ROS play an essential role in the induction of apoptosis by pristimerin in HepG2 cells.


PubMed | Wuhai Municipal Peoples Hospital
Type: Journal Article | Journal: Journal of B.U.ON. : official journal of the Balkan Union of Oncology | Year: 2013

To investigate the anticancer properties implicated in a natural triterpenoid (pristimerin)-induced apoptosis and inhibited proliferation in human hepatocellular carcinoma (HCC) HepG2 cell line.The cytotoxic activity of pristimerin in HepG2 cells was determined by MTT assay. Apoptotic morphology was observed by fluorescence microscope with Hoechst 33258 staining and percent apoptosis was measured by annexin V/PI double staining. DiOC6 for mitochondrial potential (m) and DCFH-DA for reactive oxygen species (ROS) were determined by flow cytometry. Changes of apoptotic- related proteins were analysed by Western blot.Pristimerin exerted a potent cytotoxic effect on HepG2 cells. After HepG2 cells were treated with pristimerin, typical apoptotic bodies, increasing the proportion of apoptotic annexin V-positive cells and activation of caspase-3 were detected in a dose-dependent manner. It was intriguing that pristimerin increased the generation of ROS with a collapse of the mitochondrial membrane potential in the cells. In addition, there was significant change in other mitochondrial membrane proteins triggered by pristimerin, such as Bcl-2 and Bax. Pristimerin also effectively induced subsequent release of cytochrome C from mitochondria into the cytosol, downregulated EGFR protein expression and inhibited downstream signaling pathways in HepG2 cells. Pretreatment with N-acetylcysteine (NAC) blocked ROS generation and resulted in loss of mitochondrial membrane potential, release of cytochrome C and apoptosis induced by pristimerin.These data indicate that ROS play an essential role in the induction of apoptosis by pristimerin in HepG2 cells.

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