scholarly journals Gamma linolic acid regulates PHD2 mediated hypoxia and mitochondrial apoptosis in DEN induced Hepatocellular carcinoma

2018 ◽  
Vol Volume 12 ◽  
pp. 4241-4252 ◽  
Author(s):  
Hong Cui ◽  
Feng Han ◽  
Ling Zhang ◽  
Li Wang ◽  
Mukesh Kumar
Keyword(s):  
Hepatocellular Carcinoma ◽  
Mitochondrial Apoptosis ◽  
Linolic Acid

scholarly journals microRNA-26a induces a mitochondrial apoptosis mediated by p53 through targeting to inhibit Mcl1 in human hepatocellular carcinoma

2018 ◽  
Vol Volume 11 ◽  
pp. 2227-2239 ◽  
Author(s):  
Xiao-Mei Gao ◽  
Ying Zhu ◽  
Jian-Hua Li ◽  
Xiang-Yu Wang ◽  
Xiao-Fei Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Human Hepatocellular Carcinoma ◽  
Mitochondrial Apoptosis

scholarly journals Gan-Qing-Ning Formula Inhibits the Growth of Hepatocellular Carcinoma by Promoting Apoptosis and Inhibiting Angiogenesis in H22 Tumor-Bearing Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Fan-Yan Zeng ◽  
Kai-Li Zhao ◽  
Le-Zhen Lin ◽  
Ying Deng ◽  
Si Qin ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Effect ◽  
Caspase 3 ◽  
Tumor Tissue ◽  
Mitochondrial Apoptosis ◽  
Apoptosis Pathway ◽  
Expression Levels ◽  
Mitochondrial Apoptosis Pathway ◽  
Tumor Bearing ◽  
Mrna Expression Levels

Objective. Gang-Qing-Ning (GQN) is a traditional Chinese medicine formula that has been used in the treatment of hepatocellular carcinoma (HCC) in the folk population for decades. However, scientific validation is still necessary to lend credibility to the traditional use of GQN against HCC. This study investigates the antitumor effect of GQN on H22 tumor-bearing mice and its possible mechanism. Methods. Fifty H22 tumor-bearing mice were randomly assigned to five groups. Three groups were treated with high, medium, and low dosages of GQN (27.68, 13.84, and 6.92 g/kg, respectively); the positive control group was treated with cytoxan (CTX) (20 mg/kg) and the model group was treated with normal saline. After 10 days’ treatment, the tumor inhibitory rates were calculated. Pathological changes in tumor tissue were observed, and the key proteins and genes of the mitochondrial apoptosis pathway were measured, as well as the mRNA expression levels of VEGF in tumor tissue. Results. The tumor inhibitory rates of high, medium, and low dosages of GQN groups were 47.39%, 38.26%, and 22.17%, respectively. The high dosage of the GQN group significantly increased the protein and mRNA expression levels of Bax, Cyt-C, and cleaved Caspase 3 (or Caspase 3) (P<0.01) but decreased the expression levels of Bcl-2, VEGF, and microvessel density (MVD) (P<0.01). Conclusions. The high dosage of GQN can significantly inhibit the tumor growth in H22 tumor-bearing mice. It exerts the antitumor effect by enhancing proapoptotic factors and inhibiting the antiapoptotic factor of the mitochondrial apoptosis pathway and inhibiting tumor angiogenesis.

scholarly journals B4G2 Induces Mitochondrial Apoptosis by the ROS-Mediated Opening of Ca2+-Dependent Permeability Transition Pores

2015 ◽  
Vol 37 (3) ◽  
pp. 838-852 ◽  
Author(s):  
Nan Yao ◽  
Ying-Jie Li ◽  
Dong-Mei Zhang ◽  
Dao-Lu Liu ◽  
Ming-Kuen Tang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Intracellular Calcium ◽  
Cell Lines ◽  
Permeability Transition ◽  
Mitochondrial Apoptosis ◽  
Mitochondrial Potential ◽  
Pre Treatment ◽  
Permeability Transition Pores ◽  
Underlying Mechanisms ◽  
Induced Apoptosis

Background/Aims: Hepatocellular carcinoma (HCC) is the most common type of liver cancer. At present, only sorafenib is approved to treat HCC. In this study, we found that a 23-hydroxybetulinic acid derivative, B4G2, exhibited potent antiproliferative activity in HCC cell lines. Methods: We used four HCC cell lines (HepG2, HepG2/ADM, Hep3B and Bel-7402) to evaluate the anti-tumour activity and explore underlying mechanisms by which B4G2 induces apoptosis. Results: Among these cell lines, HepG2 showed the highest sensitivity to B4G2. HepG2 cells treated with B4G2 showed a depolarized mitochondrial membrane potential, released cytochrome c, activated caspase-9 and caspase-3 and cleaved poly ADP-ribose polymerase (PARP). However, Z-VAD-FMK, a pan-caspase inhibitor, did not attenuate B4G2-induced apoptosis, implying that the induction of mitochondrial apoptosis by B4G2 may be independent of caspases. Moreover, pre-treatment with MgCl2, a blocker of Ca2+-dependent permeability transition (PT) pores, attenuated the depolarization of the mitochondrial potential and decreased the population of apoptotic cells, indicating that B4G2-induced apoptosis was partly dependent on the opening of the Ca2+-dependent PT pores. B4G2 also increased the levels of intracellular calcium and reactive oxygen species (ROS). Furthermore, an ROS scavenger, N-acetyl-cysteine (NAC), markedly decreased the accumulation of intracellular calcium and apoptosis. Conclusion: This is the first demonstration that B4G2 inhibits the growth of HCC cells and induces mitochondrial apoptosis in hepatocellular carcinoma cells by the ROS-mediated opening of Ca2+-dependent permeability transition pores.

scholarly journals Pterostilbene inhibits hepatocellular carcinoma through p53/SOD2/ROS-mediated mitochondrial apoptosis

2016 ◽  
Vol 36 (6) ◽  
pp. 3233-3240 ◽  
Author(s):  
Liying Guo ◽  
Kai Tan ◽  
Hao Wang ◽  
Xuan Zhang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Mitochondrial Apoptosis
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