Oxaliplatin induces apoptosis in hepatocellular carcinoma cells and inhibits tumor growth

2009 ◽  
Vol 18 (11) ◽  
pp. 1595-1604 ◽  
Author(s):  
Zheng Wang ◽  
Jian Zhou ◽  
Jia Fan ◽  
Shuang-Jian Qiu ◽  
Yao Yu ◽  
...  
Hepatology ◽  
2010 ◽  
Vol 52 (3) ◽  
pp. 966-974 ◽  
Author(s):  
Serif Senturk ◽  
Mine Mumcuoglu ◽  
Ozge Gursoy-Yuzugullu ◽  
Burcu Cingoz ◽  
Kamil Can Akcali ◽  
...  

2021 ◽  
Vol 19 (12) ◽  
pp. 2483-2489
Author(s):  
Li Zhuo Han ◽  
Changgao Jiang ◽  
Chunliu Mi ◽  
Ke Si Wang ◽  
Hong Xiang Zuo ◽  
...  

Purpose: To investigate the effect of excisanin A on human hepatocellular carcinoma cells as well as to elucidate its mechanism of action. Methods: Molecular docking was used to determine the binding characteristics of excisanin A to HIF-1α protein. The transcriptional activation and viability of excisanin A were assessed using Luciferase reporter and MTT assay. The HIF-1α protein in the nucleus was assayed using western blot and immunofluorescence. HIF-1α and VEGF mRNA levels were evaluated using reverse-transcription polymerase chain reaction (RT-PCR). Cell proliferation was determined by flow cytometry, as well as by EdU and clonogenic assays. In vivo tumor growth was assessed in a murine xenograft model of SKHep1 cells. Results: Excisanin A inhibited HIF-1α transcriptional activation, as well as HIF-1α protein synthesis (p < 0.001). Excisanin A also reduced VEGF protein and mRNA expressions (p < 0.001). In addition, the compound inhibited the proliferation of hepatocellular carcinoma cells. and tumor growth in the xenograft tumor model. Conclusion: Excisanin A is a potent HIF-1α inhibitor, supporting its potential development for human hepatoma therapy. Keywords: Excisanin A, HIF-1α, Protein synthesis, Hepatoma therapy


2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Chieh-Fang Cheng ◽  
I-Huang Lu ◽  
Hsiang-Wen Tseng ◽  
Chung-Yuan Sun ◽  
Li-Tsen Lin ◽  
...  

Cortex periplocae is the dried root bark ofPeriploca sepiumBge., a traditional Chinese herb medicine. It contains high amounts of cardiac glycosides. Several cardiac glycosides have been reported to inhibit tumor growth or induce tumor cell apoptosis. We extracted and purified cortex periplocae and identified periplocin as the active ingredient that inhibited the growth of TNF-related apoptosis-inducing ligand-(TRAIL-) resistant hepatocellular carcinoma cells. The antitumor activity of periplocin was further increased by TRAIL cotreatment. Periplocin sensitized TRAIL-resistant HCC through the following two mechanisms. First, periplocin induced the expression of DR4 and FADD. Second, the cotreatment of TRAIL and periplocin suppressed several inhibitors of apoptosis (IAPs). Both mechanisms resulted in the activation of caspase 3, 8, and 9 and led to cell apoptosis. In addition, intraperitoneal injection (IP) of periplocin repressed the growth of hepatocellular carcinoma (HCC) in xenograft tumor model in mice. In summary, periplocin sensitized TRAIL-resistant HCC cells to TRAIL treatment and resulted in tumor cell apoptosis and the repression of tumor growthin vivo.


Sign in / Sign up

Export Citation Format

Share Document