Agrimonia pilosa ethanol extract induces apoptotic cell death in HepG2 cells

2011 ◽  
Vol 138 (2) ◽  
pp. 358-363 ◽  
Author(s):  
Kyoung Jin Nho ◽  
Jin Mi Chun ◽  
Ho Kyoung Kim
Keyword(s):  
Cell Death ◽  
Hepg2 Cells ◽  
Apoptotic Cell ◽  
Ethanol Extract ◽  
Apoptotic Cell Death

scholarly journals O-GlcNAc Transferase Inhibitor Synergistically Enhances Doxorubicin-Induced Apoptosis in HepG2 Cells

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3154
Author(s):  
Su Jin Lee ◽  
Oh-Shin Kwon
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Hepg2 Cells ◽  
Drug Targets ◽  
Apoptotic Cell ◽  
Chemotherapy Resistance ◽  
Apoptotic Cell Death ◽  
Induced Apoptosis ◽  
Glcnac Transferase

The combination of chemotherapy with chemosensitizing agents is a common approach to enhance anticancer activity while reducing the dose-dependent adverse side effects of cancer treatment. Herein, we investigated doxorubicin (DOX) and O-GlcNAc transferase (OGT) inhibitor OSMI-1 combination treatment, which significantly enhanced apoptosis in hepatocellular carcinoma cells (HepG2) as a result of synergistic drug action in disparate stress signaling pathways. Treatment with a low dose of DOX or a suboptimal dose of OSMI-1 alone did not induce apoptotic cell death in HepG2 cells. However, the combination of DOX with OSMI-1 in HepG2 cells synergistically increased apoptotic cell death through the activation of both the p53 and mitochondrial Bcl2 pathways compared to DOX alone. We also demonstrated that the combination of DOX and OSMI-1 stimulated cell death, dramatically reducing cell proliferation and tumor growth in vivo using a HepG2 xenograft mouse model. These findings indicate that OSMI-1 acts as a potential chemosensitizer by enhancing DOX-induced cell death. This study provides insight into a possible mechanism of chemotherapy resistance, identifies potential novel drug targets, and suggests that OGT inhibition could be utilized in clinical applications to treat hepatocellular carcinoma as well as other cancer types.

Inhibition of cytochrome P450 2J2 by tanshinone IIA induces apoptotic cell death in hepatocellular carcinoma HepG2 cells

2015 ◽  
Vol 764 ◽  
pp. 480-488 ◽  
Author(s):  
Yu Jin Jeon ◽  
Joong Sun Kim ◽  
Geun Hye Hwang ◽  
Zhexue Wu ◽  
Ho Jae Han ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Death ◽  
Cytochrome P450 ◽  
Hepg2 Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Tanshinone Iia

Su1211 The Autophagy Produced by Azathioprine in HEPG2 Cells Leads to Apoptotic Cell Death Due to Inhibition With Bafilomycin A1

2012 ◽  
Vol 142 (5) ◽  
pp. S-452
Author(s):  
Borja Hernandez-Breijo ◽  
I.D. Roman ◽  
Dolores Fernandez-Moreno ◽  
Jorge Monserrat ◽  
Javier P. Gisbert ◽  
...  
Keyword(s):  
Cell Death ◽  
Hepg2 Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Bafilomycin A1

scholarly journals Phyllanthin prevents diethylnitrosamine (DEN) induced liver carcinogenesis in rats and induces apoptotic cell death in HepG2 cells

2021 ◽  
Vol 137 ◽  
pp. 111335
Author(s):  
Yulai You ◽  
Fengfeng Zhu ◽  
Zhenhuan Li ◽  
LingFeng Zhang ◽  
Yu Xie ◽  
...  
Keyword(s):  
Cell Death ◽  
Hepg2 Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Liver Carcinogenesis

scholarly journals Chemical Constituent Profiling of Phyllostachys heterocycla var. Pubescens with Selective Cytotoxic Polar Fraction through EGFR Inhibition in HepG2 Cells

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 940
Author(s):  
Reda F. A. Abdelhameed ◽  
Eman S. Habib ◽  
Ahmed K. Ibrahim ◽  
Koji Yamada ◽  
Maged S. Abdel-Kader ◽  
...  
Keyword(s):  
Cell Death ◽  
Hepg2 Cells ◽  
Cell Cycle Progression ◽  
Kinase Inhibitor ◽  
Apoptotic Cell ◽  
Chemical Constituent ◽  
Apoptotic Cell Death ◽  
Egfr Inhibition ◽  
In Silico Studies ◽  
Phyllostachys Heterocycla

Different extracts of the Bamboo shoot skin Phyllostachys heterocycla var. pubescens were screened against panel of cancer cell lines and normal one. The cell viability results exhibited that the ethyl acetate extract showed the least vitality percentage of 2.14% of HepG2 cells. Accordingly, it was subjected to chromatographic separation, which resulted in the isolation of a new natural product; 7-hydroxy, 5-methoxy, methyl cinnamate (1), together with four known compounds. The structures of the pure isolated compounds were deduced based on different spectroscopic data. The new compound (1) was screened against the HepG2 and MCF-7 cells and showed IC50 values of 7.43 and 10.65 µM, respectively. It induced apoptotic cell death in HepG2 with total apoptotic cell death of 58.6% (12.44-fold) compared to 4.71% in control by arresting cell cycle progression at the G1 phase. Finally, compound 1 was validated as EGFR tyrosine kinase inhibitor in both enzymatic levels (IC50 = 98.65 nM compared to Erlotinib (IC50 = 78.65 nM). Finally, in silico studies of compound 1 through the molecular docking indicated its high binding affinity towards EGFR protein and the ADME pharmacokinetics indicated it as a drug-like.

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