scholarly journals Potent antitumor activity of oncolytic adenovirus-mediated SOCS1 for hepatocellular carcinoma

Gene Therapy ◽  
2012 ◽  
Vol 20 (1) ◽  
pp. 84-92 ◽  
Author(s):  
L Liu ◽  
W Li ◽  
X Wei ◽  
Q Cui ◽  
W Lou ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Activity ◽  
Oncolytic Adenovirus

Significant antitumor activity of oncolytic adenovirus expressing human interferon-β for hepatocellular carcinoma

2008 ◽  
Vol 10 (9) ◽  
pp. 983-992 ◽  
Author(s):  
Ling Feng He ◽  
Jin Fa Gu ◽  
Wen Hao Tang ◽  
Jun Kai Fan ◽  
Na Wei ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Activity ◽  
Oncolytic Adenovirus ◽  
Human Interferon ◽  
Interferon Β

Potent antitumor activity of oncolytic adenovirus expressing C/EBPβ against hepatocellular carcinoma

APOPTOSIS ◽  
2020 ◽  
Vol 25 (3-4) ◽  
pp. 154-156
Author(s):  
Yan Zeng ◽  
Feng-di Li ◽  
Jiang-long Du ◽  
Yu-jia Xue ◽  
Jing Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Activity ◽  
Oncolytic Adenovirus

The Effect and Mechanism of Apoptosis Induced by Desacetylcinobufotalin (DEBF) in Human Hepatocellular Carcinoma HepG2 Cells

2013 ◽  
Vol 395-396 ◽  
pp. 587-590
Author(s):  
Xu Chao ◽  
Lin Dang ◽  
Min Hui Wei
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Activity ◽  
Western Blot ◽  
Hepg2 Cells ◽  
Human Hepatocellular Carcinoma ◽  
Inhibition Effect ◽  
Marked Inhibition ◽  
Mitochondria Pathway

The cytotoxicity of Desacetylcinobufotalin (DEBF) and apoptosis induced by DEBF was measured. Additionally the mechanism of Apoptosis induced by DEBF was studied through Western blot. The results show DEBF displayed the marked inhibition effect to HepG2 cells and the IC50value is 0.0279μmol/ml. The expression of Bax was significantly increased and the expression of Bcl-2 was markedly decreased, compared to the control. The data suggest DEBF had significant antitumor activity through induction apoptosis via mitochondria pathway.

Antitumor activity of tatariside F isolated from roots of Fagopyrum tataricum (L.) Gaertn against H22 hepatocellular carcinoma via up-regulation of p53

Phytomedicine ◽  
2015 ◽  
Vol 22 (7-8) ◽  
pp. 730-736 ◽  
Author(s):  
Wei Peng ◽  
Changling Hu ◽  
Zhiheng Shu ◽  
Ting Han ◽  
Luping Qin ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Antitumor Activity ◽  
Fagopyrum Tataricum

scholarly journals Positively Charged Nanoparticle Delivery of n-Butylidenephthalide Enhances Antitumor Effect in Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Kai-Fu Chang ◽  
Xiao-Fan Huang ◽  
Yu-Ling Lin ◽  
Kuang-Wen Liao ◽  
Ming-Chang Hsieh ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Antitumor Activity ◽  
Cell Apoptosis ◽  
Cell Uptake ◽  
Cell Cycle Regulators ◽  
Clinical Drug Development ◽  
Apoptosis Pathways ◽  
Clinical Drug ◽  
Hcc Cells

Hepatocellular carcinoma (HCC) is the second and sixth leading cause of cancer death in men and woman in 185 countries statistics, respectively. n-Butylidenephthalide (BP) has shown anti-HCC activity, but it also has an unstable structure that decreases its potential antitumor activity. The aim of this study was to investigate the cell uptake, activity protection, and antitumor mechanism of BP encapsulated in the novel liposome LPPC in HCC cells. BP/LPPC exhibited higher cell uptake and cytotoxicity than BP alone, and combined with clinical drug etoposide (VP-16), BP/LPPC showed a synergistic effect against HCC cells. Additionally, BP/LPPC increased cell cycle regulators (p53, p-p53, and p21) and decreased cell cycle-related proteins (Rb, p-Rb, CDK4, and cyclin D1), leading to cell cycle arrest at the G0/G1 phase in HCC cells. BP/LPPC induced cell apoptosis through activation of both the extrinsic (Fas-L and Caspase-8) and intrinsic (Bax and Caspase-9) apoptosis pathways and activated the caspase cascade to trigger HCC cell death. In conclusion, the LPPC complex improved the antitumor activity of BP in terms of cytotoxicity, cell cycle regulation and cell apoptosis, and BP/LPPC synergistically inhibited cell growth during combination treatment with VP-16 in HCC cells. Therefore, BP/LPPC is potentially a good candidate for clinical drug development or for use as an adjuvant for clinical drugs as a combination therapy for hepatocellular carcinoma.

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